PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17873517-6 2007 In addition, indomethacin decreased the expression of NFkappaB-regulated gene products involved in rhLTalpha-induced anti-apoptosis (XIAP, cFLIP and cIAP-1), which may explain its sensitization of tumor cells to rhLTalpha and/or cisplatin/adriamycin. Cisplatin 229-238 nuclear factor kappa B subunit 1 Homo sapiens 54-62 17131310-4 2007 Mechanistically, genistein augmented cisplatin induced killing by down regulating transcription factor-NF-kappaB and anti-apoptotic Akt expression. Cisplatin 37-46 nuclear factor kappa B subunit 1 Homo sapiens 103-112 17516123-0 2007 Cisplatin cytotoxicity of auditory cells requires secretions of proinflammatory cytokines via activation of ERK and NF-kappaB. Cisplatin 0-9 nuclear factor kappa B subunit 1 Homo sapiens 116-125 17516123-2 2007 In this study, we demonstrate that cisplatin increased the early immediate release and de novo synthesis of proinflammatory cytokines, including TNF-alpha, IL-1beta, and IL-6, through the activation of ERK and NF-kappaB in HEI-OC1 cells, which are conditionally immortalized cochlear cells that express hair cell markers. Cisplatin 35-44 nuclear factor kappa B subunit 1 Homo sapiens 210-219 17586463-0 2007 Epstein-Barr virus-encoded LMP1 promotes cisplatin-induced caspase activation through JNK and NF-kappaB signaling pathways. Cisplatin 41-50 nuclear factor kappa B subunit 1 Homo sapiens 94-103 17586463-3 2007 CTAR2 is known to engage the c-Jun N-terminal kinase (JNK) and NF-kappaB pathways, and we show here that SP600125, a selective JNK inhibitor, suppresses LMP1 potentiation of cisplatin-induced mitochondrial damage and caspase activation in HeLa cells. Cisplatin 174-183 nuclear factor kappa B subunit 1 Homo sapiens 63-72 17586463-4 2007 Moreover, the potentiation of cisplatin-triggered caspase activation was blocked by Bay11-7082, a potent inhibitor of NF-kappaB. Cisplatin 30-39 nuclear factor kappa B subunit 1 Homo sapiens 118-127 17308110-7 2007 We also show that down-regulation of NF-kappaB via Aurora-A depletion can enhance cisplatin-dependent apoptosis. Cisplatin 82-91 nuclear factor kappa B subunit 1 Homo sapiens 37-46 17131310-5 2007 NF-kappaB was found upregulated when pancreatic cancer cells were exposed to cisplatin, suggesting the potential mechanism of acquired chemo-resistance. Cisplatin 77-86 nuclear factor kappa B subunit 1 Homo sapiens 0-9 17131310-7 2007 But most importantly, our data also showed that a specific target, such as NF-kappaB, was inactivated in animal tumors treated with genistein and cisplatin. Cisplatin 146-155 nuclear factor kappa B subunit 1 Homo sapiens 75-84 17131310-9 2007 These results provide strong molecular in vivo evidence in support of our hypothesis that inactivation of the NF-kappaB signaling pathway by genistein results in the chemo-sensitization of pancreatic tumors to cisplatin, which is likely to be an important and novel strategy for the treatment of pancreatic cancer. Cisplatin 210-219 nuclear factor kappa B subunit 1 Homo sapiens 110-119 16613577-5 2006 Recently, we found that genistein sensitized cancer cells to apoptosis induced by chemotherapeutic agents including docetaxel, gemcitabine and cisplatin through inactivation of NF-kappaB in multiple cancer cell lines. Cisplatin 143-152 nuclear factor kappa B subunit 1 Homo sapiens 177-186 16461557-0 2006 Glucocorticoids enhance cytotoxicity of cisplatin via suppression of NF-{kappa}B activation in the glucocorticoid receptor-rich human cervical carcinoma cell line SiHa. Cisplatin 40-49 nuclear factor kappa B subunit 1 Homo sapiens 69-80 16475211-3 2006 In the current study, they focused their investigation on testing whether the inactivation of NF-kappaB by genistein could enhance cisplatin-induced cell growth inhibition and apoptosis in BxPC-3 cells in vitro and antitumor activity of cisplatin in vivo. Cisplatin 131-140 nuclear factor kappa B subunit 1 Homo sapiens 94-103 16475211-9 2006 Preexposure of BxPC-3 cells to genistein abrogated cisplatin-induced activation of NF-kappaB, which appeared to be consistent with the authors" hypothesis. Cisplatin 51-60 nuclear factor kappa B subunit 1 Homo sapiens 83-92 16475211-12 2006 Most important, for the first time, the authors observed that the DNA-binding activity of NF-kappaB was inactivated in genistein-treated animal tumors, whereas cisplatin significantly induced NF-kappaB DNA binding activity, and this was completely abrogated in genistein-pretreated tumors that were exposed to cisplatin, consistent with the in vitro data. Cisplatin 160-169 nuclear factor kappa B subunit 1 Homo sapiens 192-201 16475211-12 2006 Most important, for the first time, the authors observed that the DNA-binding activity of NF-kappaB was inactivated in genistein-treated animal tumors, whereas cisplatin significantly induced NF-kappaB DNA binding activity, and this was completely abrogated in genistein-pretreated tumors that were exposed to cisplatin, consistent with the in vitro data. Cisplatin 310-319 nuclear factor kappa B subunit 1 Homo sapiens 90-99 16461557-4 2006 In this study, we found that this cisplatin cytotoxicity-enhancing effect of DEX correlated well with its effect on abrogating the cisplatin-induced activation of nuclear factor kappa B (NF-kappaB). Cisplatin 34-43 nuclear factor kappa B subunit 1 Homo sapiens 163-185 16461557-4 2006 In this study, we found that this cisplatin cytotoxicity-enhancing effect of DEX correlated well with its effect on abrogating the cisplatin-induced activation of nuclear factor kappa B (NF-kappaB). Cisplatin 34-43 nuclear factor kappa B subunit 1 Homo sapiens 187-196 16461557-4 2006 In this study, we found that this cisplatin cytotoxicity-enhancing effect of DEX correlated well with its effect on abrogating the cisplatin-induced activation of nuclear factor kappa B (NF-kappaB). Cisplatin 131-140 nuclear factor kappa B subunit 1 Homo sapiens 163-185 16461557-4 2006 In this study, we found that this cisplatin cytotoxicity-enhancing effect of DEX correlated well with its effect on abrogating the cisplatin-induced activation of nuclear factor kappa B (NF-kappaB). Cisplatin 131-140 nuclear factor kappa B subunit 1 Homo sapiens 187-196 16461557-7 2006 Our data suggest that the specific action of DEX on GR may enhance the cytotoxicity of cisplatin in selected GR-rich cancer cells by suppressing NF-kappaB activation. Cisplatin 87-96 nuclear factor kappa B subunit 1 Homo sapiens 145-154 16424027-4 2006 Similar to other genotoxic agents, such as daunorubicin and UV light, cisplatin treatment in the U-2 OS osteosarcoma cell line represses RelA activity and inhibits expression of the NF-kappaB antiapoptotic target gene Bcl-x(L). Cisplatin 70-79 nuclear factor kappa B subunit 1 Homo sapiens 182-191 16061678-9 2005 Moreover, we found that the NF-kappaB activity was significantly increased within 2 hours of cisplatin and docetaxel treatment and that the NF-kappaB inducing activity of these agents was completely abrogated in cells pretreated with genistein. Cisplatin 93-102 nuclear factor kappa B subunit 1 Homo sapiens 28-37 16044419-0 2005 Biological and chemical inhibitors of NF-kappaB sensitize SiHa cells to cisplatin-induced apoptosis. Cisplatin 72-81 nuclear factor kappa B subunit 1 Homo sapiens 38-47 16044419-6 2005 Cisplatin induced NF-kappaB DNA binding activity in HeLa and SiHa cells but not in primary cervical cells and the active DNA binding complex in SiHa cells consists of p50 and RelA heterodimers. Cisplatin 0-9 nuclear factor kappa B subunit 1 Homo sapiens 18-27 16044419-6 2005 Cisplatin induced NF-kappaB DNA binding activity in HeLa and SiHa cells but not in primary cervical cells and the active DNA binding complex in SiHa cells consists of p50 and RelA heterodimers. Cisplatin 0-9 nuclear factor kappa B subunit 1 Homo sapiens 167-170 16044419-7 2005 However, when NF-kappaB DNA binding activity was blocked by chemical (curcumin, PDTC, or salicylic acid) or biological inhibitors (NIK-KM or IKK-beta DN), the cell viability was less in SiHa cells with cisplatin treatment, but these effects were not observed in HeLa cells. Cisplatin 202-211 nuclear factor kappa B subunit 1 Homo sapiens 14-23 16044419-8 2005 Similarly upon treatment with cisplatin SiHa cells had more activation of caspases compared to that seen in HeLa cells under conditions of NF-kappaB inhibition by biological or chemical inhibitors. Cisplatin 30-39 nuclear factor kappa B subunit 1 Homo sapiens 139-148 16044419-9 2005 These results suggest that NF-kappaB may contribute to the resistance of human cervical cancer cells to cisplatin and highlight the potential use of combination therapy involving cisplatin and NF-kappaB inhibitors. Cisplatin 104-113 nuclear factor kappa B subunit 1 Homo sapiens 27-36 16044419-9 2005 These results suggest that NF-kappaB may contribute to the resistance of human cervical cancer cells to cisplatin and highlight the potential use of combination therapy involving cisplatin and NF-kappaB inhibitors. Cisplatin 179-188 nuclear factor kappa B subunit 1 Homo sapiens 27-36 15073167-0 2004 Suppression of MEK/ERK signaling pathway enhances cisplatin-induced NF-kappaB activation by protein phosphatase 4-mediated NF-kappaB p65 Thr dephosphorylation. Cisplatin 50-59 nuclear factor kappa B subunit 1 Homo sapiens 68-77 15246562-0 2004 Up-regulation of Bfl-1/A1 via NF-kappaB activation in cisplatin-resistant human bladder cancer cell line. Cisplatin 54-63 nuclear factor kappa B subunit 1 Homo sapiens 30-39 15246562-7 2004 The nuclear translocation of nuclear factor-kappaB (NF-kappaB) by cisplatin and gamma-irradiation selectively occurred in T24R2 cells. Cisplatin 66-75 nuclear factor kappa B subunit 1 Homo sapiens 29-50 15246562-7 2004 The nuclear translocation of nuclear factor-kappaB (NF-kappaB) by cisplatin and gamma-irradiation selectively occurred in T24R2 cells. Cisplatin 66-75 nuclear factor kappa B subunit 1 Homo sapiens 52-61 15246562-10 2004 Our findings suggest that the induction of Bfl-1/A1 by NF-kappaB may be important in controlling resistance to cisplatin responses in bladder tumor cells. Cisplatin 111-120 nuclear factor kappa B subunit 1 Homo sapiens 55-64 15073167-3 2004 Pretreatment of SiHa cells with MEK/ERK inhibitor enhanced cisplatin-induced NF-kappaB activation. Cisplatin 59-68 nuclear factor kappa B subunit 1 Homo sapiens 77-86 15073167-4 2004 However, results of immunoblotting analysis showed that neither cisplatin nor MEK/ERK inhibitors induced marked IkappaBalpha degradation, suggesting that suppression of the MEK/ERK signaling pathway may enhance cisplatin-induced NF-kappaB activation via mechanisms other than the conventional pathway. Cisplatin 211-220 nuclear factor kappa B subunit 1 Homo sapiens 229-238 15073167-6 2004 Coincident with activation of NF-kappaB, cisplatin induced Ser phosphorylation but decreased Thr phosphorylation of NF-kappaB p65. Cisplatin 41-50 nuclear factor kappa B subunit 1 Homo sapiens 30-39 15073167-6 2004 Coincident with activation of NF-kappaB, cisplatin induced Ser phosphorylation but decreased Thr phosphorylation of NF-kappaB p65. Cisplatin 41-50 nuclear factor kappa B subunit 1 Homo sapiens 116-125 15026414-6 2004 Inhibition of NFkappaB activity either by treatment with the IkappaBalpha phosphorylation inhibitor (BAY 11-7085) or a specific NFkappaB nuclear translocation inhibitor (SN-50) or by transfection of p50DeltaNLS (which lacks the nuclear localization signal domain) increased the efficacy of both the cisplatin-induced attenuation of IkappaBalpha phosphorylation and NFkappaB activity and the cisplatin-induced apoptosis. Cisplatin 299-308 nuclear factor kappa B subunit 1 Homo sapiens 14-22 15073167-10 2004 PP4-overexpressing cells showed a decrease in Thr phosphorylation of NF-kappaB p65 to nearly undetectable levels, and both basal and cisplatin-induced NF-kappaB activities were higher than those in parental cells. Cisplatin 133-142 nuclear factor kappa B subunit 1 Homo sapiens 151-160 15026414-6 2004 Inhibition of NFkappaB activity either by treatment with the IkappaBalpha phosphorylation inhibitor (BAY 11-7085) or a specific NFkappaB nuclear translocation inhibitor (SN-50) or by transfection of p50DeltaNLS (which lacks the nuclear localization signal domain) increased the efficacy of both the cisplatin-induced attenuation of IkappaBalpha phosphorylation and NFkappaB activity and the cisplatin-induced apoptosis. Cisplatin 391-400 nuclear factor kappa B subunit 1 Homo sapiens 14-22 15026414-9 2004 These results suggest that combination therapy of cisplatin with the NFkappaB inhibitor should increase the therapeutic efficacy of cisplatin. Cisplatin 50-59 nuclear factor kappa B subunit 1 Homo sapiens 69-77 15026414-9 2004 These results suggest that combination therapy of cisplatin with the NFkappaB inhibitor should increase the therapeutic efficacy of cisplatin. Cisplatin 132-141 nuclear factor kappa B subunit 1 Homo sapiens 69-77 12871783-8 2003 These data demonstrated that ad-IkappaBalpha blockade of chemotherapeutic induced NF-kappaB activation increased apoptosis induction and the chemosensitivity of lung cancer cell lines with acquired resistance to cisplatin and adriamycin. Cisplatin 212-221 nuclear factor kappa B subunit 1 Homo sapiens 82-91 15097869-10 2004 Moreover, the NF-kappaB activity was significantly increased within 2 hours of docetaxel or cisplatin treatment, and the NF-kappaB-inducing activity of these agents was completely abrogated in cells pretreated with genistein. Cisplatin 92-101 nuclear factor kappa B subunit 1 Homo sapiens 14-23 15097869-11 2004 These results clearly suggest that genistein pretreatment, which inactivates NF-kappaB activity, together with other cellular effects of genistein, may contribute to increased cell growth inhibition and apoptosis inducing effects of nontoxic doses of docetaxel and cisplatin, which could be a novel strategy for the treatment of pancreatic cancer. Cisplatin 265-274 nuclear factor kappa B subunit 1 Homo sapiens 77-86 15026414-0 2004 Inhibition of NFkappaB increases the efficacy of cisplatin in in vitro and in vivo ovarian cancer models. Cisplatin 49-58 nuclear factor kappa B subunit 1 Homo sapiens 14-22 15026414-2 2004 We compared the basal levels of phosphorylation of IkappaBalpha and activity of NFkappaB between cisplatin-sensitive A2780 cells and cisplatin-resistant Caov-3 cells. Cisplatin 97-106 nuclear factor kappa B subunit 1 Homo sapiens 80-88 15026414-4 2004 Cisplatin caused a more marked decrease in the phosphorylation of IkappaBalpha and activity of NFkappaB in A2780 cells than in Caov-3 cells. Cisplatin 0-9 nuclear factor kappa B subunit 1 Homo sapiens 95-103 15026414-5 2004 Thus, high basal levels of phosphorylation of IkappaBalpha and activation of NFkappaB and less marked inhibition of the phosphorylation of IkappaBalpha and activation of NFkappaB by cisplatin seem to reduce the sensitivity of cells to cisplatin. Cisplatin 182-191 nuclear factor kappa B subunit 1 Homo sapiens 170-178 12871783-4 2003 In this study, we transferred the "super-repressor" form of the NF-kappaB inhibitor by adenoviral vector (ad-IkappaBalpha) to human lung cancer cell lines with resistant to cisplatin (PC-14-DDP) and adriamycin (PC-14-ADR), and observed the sensitivity change. Cisplatin 173-182 nuclear factor kappa B subunit 1 Homo sapiens 64-73 12871783-5 2003 Electrophoretic mobility shift assay showed that ad-IkappaBalpha blocked the activation of NF-kappaB induced by cisplatin and adriamycin. Cisplatin 112-121 nuclear factor kappa B subunit 1 Homo sapiens 91-100 11996883-0 2002 Increase of the resistance of human cervical carcinoma cells to cisplatin by inhibition of the MEK to ERK signaling pathway partly via enhancement of anticancer drug-induced NF kappa B activation. Cisplatin 64-73 nuclear factor kappa B subunit 1 Homo sapiens 174-184 12618201-3 2003 We examined the molecular mechanisms involved in the induction of apoptosis by CDDP as regards both suppression of NF-kappaB and activation of caspases. Cisplatin 79-83 nuclear factor kappa B subunit 1 Homo sapiens 115-124 11996883-3 2002 Both cisplatin and doxorubicin activated nuclear ERK2 and nuclear transcription factor kappa B (NF kappa B) of SiHa cells. Cisplatin 5-14 nuclear factor kappa B subunit 1 Homo sapiens 96-106 11942326-4 2002 Here we demonstrate that cisplatin (CDDP) and etoposide (VP-16) induce nuclear translocation of NF-kappaB in prostate cancer cell lines, followed by secretion of IL-6. Cisplatin 25-34 nuclear factor kappa B subunit 1 Homo sapiens 96-105 11996883-4 2002 However, suppression of the MEK-ERK2 pathway by PD98059 resulted in a further enhancement of cisplatin-induced NF kappa B activation, while no further regulation of NF kappa B was noted in doxorubicin-treated cells. Cisplatin 93-102 nuclear factor kappa B subunit 1 Homo sapiens 111-121 11996883-5 2002 The activation of NF kappa B by cisplatin or doxorubicin was not due to the degradation of cytoplasmic I kappa B alpha, as demonstrated by western blotting. Cisplatin 32-41 nuclear factor kappa B subunit 1 Homo sapiens 18-28 11996883-7 2002 Our results suggest that the MEK-ERK signaling pathway plays a role in the chemosensitivity of SiHa cells, and suppression of this pathway increases cisplatin resistance partly via an increase of NF kappa B activation. Cisplatin 149-158 nuclear factor kappa B subunit 1 Homo sapiens 196-206 11942326-4 2002 Here we demonstrate that cisplatin (CDDP) and etoposide (VP-16) induce nuclear translocation of NF-kappaB in prostate cancer cell lines, followed by secretion of IL-6. Cisplatin 36-40 nuclear factor kappa B subunit 1 Homo sapiens 96-105 10362102-10 1999 These findings indicate that treatment with CDDP and 5-FU induces ICAM-1 expression by a NF-kappaB independent regulatory mechanism involving PTK. Cisplatin 44-48 nuclear factor kappa B subunit 1 Homo sapiens 89-98 11084634-0 2000 Cisplatin and radiation sensitivity in human head and neck squamous carcinomas are independently modulated by glutathione and transcription factor NF-kappaB. Cisplatin 0-9 nuclear factor kappa B subunit 1 Homo sapiens 147-156 11084634-4 2000 METHODS: We examined human HNSCC lines to define the relationship of cisplatin and radiation sensitivity to intracellular GSH and NF-kappaB and determined whether HNSCC could be sensitized to these modalities by lowering the concentration of glutathione with L-buthionine sulfoximine or inhibiting activation of NF-kappaB by expression of a degradation-resistant mutant inhibitor-kappaBalpha. Cisplatin 69-78 nuclear factor kappa B subunit 1 Homo sapiens 130-139 11225847-0 2000 IkappaB/NF-kappaB mediated cisplatin resistance in HeLa cells after low-dose gamma-irradiation is associated with altered SODD expression. Cisplatin 27-36 nuclear factor kappa B subunit 1 Homo sapiens 8-17 11225847-5 2000 The translocation of NF-kappaB does not seem to be affected in a similar manner since masking of the translocation sequence by NF-kappaB SN50 enhances cisplatin toxicity to the same degree in both cell lines and overcomes drug resistance. Cisplatin 151-160 nuclear factor kappa B subunit 1 Homo sapiens 127-136 11225847-8 2000 A possible involvement of SODD in cisplatin resistance is discussed, which may shift the balance between life and death in the TNF receptor pathway to increased NF-kappaB activation. Cisplatin 34-43 nuclear factor kappa B subunit 1 Homo sapiens 161-170 11679590-11 2001 Together these findings show that NF-kappa B activation mediates doxorubicin-induced cell death without evidence of caspase function and suggest that cisplatin and doxorubicin engage different death pathways to kill neuroblastoma cells. Cisplatin 150-159 nuclear factor kappa B subunit 1 Homo sapiens 34-44 34658905-6 2021 The mechanistic studies indicated that it might alleviate CDDP-AKI by inhibiting oxidative stress, apoptosis, and IKKbeta/IkappaBalpha/p65/transcription factor nuclear kappa B (NF-kappaB) inflammation signaling pathway induced by CDDP. Cisplatin 58-62 nuclear factor kappa B subunit 1 Homo sapiens 177-186 33971703-0 2022 Enrichment of Wee1/CDC2 and NF-kappaB Signaling Pathway Constituents Mutually Contributes to CDDP Resistance in Human Osteosarcoma. Cisplatin 93-97 nuclear factor kappa B subunit 1 Homo sapiens 28-37 33971703-2 2022 Although the Wee1/CDC2 and NF-kappaB pathways were reported to show abnormal activation in some tumor cells with CDDP resistance, whether there is any concrete connection is currently unclear. Cisplatin 113-117 nuclear factor kappa B subunit 1 Homo sapiens 27-36 33971703-11 2022 Conclusion: Simultaneous enrichment of molecules in the Wee1/CDC2 and NF-kappaB pathways and their consequent coactivation is a new molecular mechanism of CDDP resistance in OS cells. Cisplatin 155-159 nuclear factor kappa B subunit 1 Homo sapiens 70-79 34935060-11 2022 Together, these findings suggest that intrinsic ROS levels were elevated by mitochondrial DNA mutations, which decreased the sensitivity to CDDP via activation of NF-kappaB signaling and induction of IAP expression in ACR20 cells. Cisplatin 140-144 nuclear factor kappa B subunit 1 Homo sapiens 163-172 34860160-16 2021 CONCLUSION: Loss of SGK1 suppresses the malignant behavior of gastric cancer cells and increases cisplatin sensitivity by restraining the NF-kappaB signaling pathway. Cisplatin 97-106 nuclear factor kappa B subunit 1 Homo sapiens 138-147 34339961-0 2021 miR-132-3p promotes the cisplatin-induced apoptosis and inflammatory response of renal tubular epithelial cells by targeting SIRT1 via the NF-kappaB pathway. Cisplatin 24-33 nuclear factor kappa B subunit 1 Homo sapiens 139-148 34339961-13 2021 Mechanistically, the SIRT1 expression was suppressed and the NF-kappaB signaling pathway was activated by the upregulation of miR-132-3p in cisplatin-induced AKI. Cisplatin 140-149 nuclear factor kappa B subunit 1 Homo sapiens 61-70 34339961-16 2021 Our results suggested that miR-132-3p exacerbated cisplatin-induced AKI by negatively regulating SIRT1 and activating the NF-kappaB signaling pathway. Cisplatin 50-59 nuclear factor kappa B subunit 1 Homo sapiens 122-131 10362102-0 1999 Synergistic induction of ICAM-1 expression by cisplatin and 5-fluorouracil in a cancer cell line via a NF-kappaB independent pathway. Cisplatin 46-55 nuclear factor kappa B subunit 1 Homo sapiens 103-112 9403032-0 1997 Modulation of NF-kappa B, and Bcl-2 in apoptosis induced by cisplatin in HeLa cells. Cisplatin 60-69 nuclear factor kappa B subunit 1 Homo sapiens 14-24 9403032-3 1997 Although AP-1 levels were not modified during cisplatin exposure, electrophoretic mobility shift assays demonstrated an increase in NF-kappa B DNA binding activity that correlated with a decrease of the inhibitory protein I kappa B alpha and a specific relocalization of c-Rel, as assessed by immunoblotting and immunofluorescence. Cisplatin 46-55 nuclear factor kappa B subunit 1 Homo sapiens 132-142 33973461-5 2021 In the combined treatment, OPZ was found to inhibit the degradation of inhibitory factor kappaB alpha induced by cisplatin, thereby inhibiting the activation of NF-kappaB, which causes cisplatin resistance, and enhancing the sensitivity of the tumor cells to cisplatin. Cisplatin 185-194 nuclear factor kappa B subunit 1 Homo sapiens 161-170 33973461-5 2021 In the combined treatment, OPZ was found to inhibit the degradation of inhibitory factor kappaB alpha induced by cisplatin, thereby inhibiting the activation of NF-kappaB, which causes cisplatin resistance, and enhancing the sensitivity of the tumor cells to cisplatin. Cisplatin 185-194 nuclear factor kappa B subunit 1 Homo sapiens 161-170 34953057-0 2022 MiR-192/NKRF axis confers lung cancer cell chemoresistance to cisplatin via the NF-kappaB pathway. Cisplatin 62-71 nuclear factor kappa B subunit 1 Homo sapiens 80-89 34953057-10 2022 Inhibition of the NF-kappaB signal pathway by curcumin reversed the effect of upregulation of miR-192 on proliferation, apoptosis and cisplatin-resistance in lung cancer cells. Cisplatin 134-143 nuclear factor kappa B subunit 1 Homo sapiens 18-27 34953057-11 2022 These results indicated that miR-192/ NKRF axis enhances the cisplatin resistance of lung cancer cells through activating the NF-kappaB pathway in vitro. Cisplatin 61-70 nuclear factor kappa B subunit 1 Homo sapiens 126-135 34558639-0 2021 miR-383 increases the cisplatin sensitivity of lung adenocarcinoma cells through inhibition of the RBM24-mediated NF-kappaB signaling pathway. Cisplatin 22-31 nuclear factor kappa B subunit 1 Homo sapiens 114-123 34790784-7 2021 Additionally, DDP treatment increased the protein phosphorylation expression of IKKbeta, JNK, ERK, and p38 in a dose-dependent manner, which was antagonized by the treatment of NF-kappaB-specific inhibitor BAY 11-7082 and pan-MAPK inhibitor U0126. Cisplatin 14-17 nuclear factor kappa B subunit 1 Homo sapiens 177-186 34658905-6 2021 The mechanistic studies indicated that it might alleviate CDDP-AKI by inhibiting oxidative stress, apoptosis, and IKKbeta/IkappaBalpha/p65/transcription factor nuclear kappa B (NF-kappaB) inflammation signaling pathway induced by CDDP. Cisplatin 230-234 nuclear factor kappa B subunit 1 Homo sapiens 177-186 34513825-8 2021 To explore possible mechanisms of IFI6 influencing OC proliferation and cisplatin resistance, GSEA is conducted and shows that IFI6 is positively correlated with the NF-kappaB pathway, which is validated by RT-qPCR. Cisplatin 72-81 nuclear factor kappa B subunit 1 Homo sapiens 166-175 34410944-0 2021 Induction of Apoptosis and Inhibition of EGFR/NF-kappaB Signaling Are Associated With Regorafenib-sensitized Non-small Cell Lung Cancer to Cisplatin. Cisplatin 139-148 nuclear factor kappa B subunit 1 Homo sapiens 46-55 34410944-5 2021 RESULTS: Cisplatin-induced epidermal growth factor receptor (EGFR)/nuclear factor kappaB (NF-kappaB) signaling was effectively inhibited by regorafenib treatment. Cisplatin 9-18 nuclear factor kappa B subunit 1 Homo sapiens 90-99 34410944-6 2021 Regorafenib, erlotinib (EGFR inhibitor) and QNZ (NF-kappaB inhibitor) may all enhance the cytotoxicity effect of cisplatin. Cisplatin 113-122 nuclear factor kappa B subunit 1 Homo sapiens 49-58 34410944-9 2021 CONCLUSION: Apoptosis induction and EGFR/NF-kappaB inactivation correlate with regorafenib-enhanced anti-NSCLC efficacy of cisplatin. Cisplatin 123-132 nuclear factor kappa B subunit 1 Homo sapiens 41-50 34094673-7 2021 Consistently, A2780 cells co-incubated with SKOV3 pretreated with an NF-kappaB inhibitor or miR-429 antagomir showed sensitivity to cisplatin and exhibited attenuated cell proliferation. Cisplatin 132-141 nuclear factor kappa B subunit 1 Homo sapiens 69-78 33617838-0 2021 Pentraxin 3 acts as a functional effector of Akt/NF-kappaB signaling to modulate the progression and cisplatin-resistance in non-small cell lung cancer. Cisplatin 101-110 nuclear factor kappa B subunit 1 Homo sapiens 49-58 34994335-10 2022 These compounds combined with cisplatin caused upregulation in the pro-apoptotic Bax, Bid, caspase-3, caspase-8, caspase-9, Fas, and p53 gene expressions while downregulating anti-apoptotic DFFA, NFkB1, and Bcl2 gene expressions. Cisplatin 30-39 nuclear factor kappa B subunit 1 Homo sapiens 196-201 34001704-14 2021 CONCLUSIONS: Emodin reverses the cisplatin resistance of tumor cells by down-regulating expression of P-gp, MRP and GST, increasing the intracellular accumulation in A549/DDP cells, and the effect may be associated with the NF-kappaB pathways. Cisplatin 33-42 nuclear factor kappa B subunit 1 Homo sapiens 224-233 35139763-0 2022 Cancer-associated fibroblast exosomes promote chemoresistance to cisplatin in hepatocellular carcinoma through circZFR targeting signal transducers and activators of transcription (STAT3)/ nuclear factor -kappa B (NF-kappaB) pathway. Cisplatin 65-74 nuclear factor kappa B subunit 1 Homo sapiens 189-212 35139763-0 2022 Cancer-associated fibroblast exosomes promote chemoresistance to cisplatin in hepatocellular carcinoma through circZFR targeting signal transducers and activators of transcription (STAT3)/ nuclear factor -kappa B (NF-kappaB) pathway. Cisplatin 65-74 nuclear factor kappa B subunit 1 Homo sapiens 214-223 33905466-0 2021 Corrigendum: Combination of Tanshinone IIA and Cisplatin Inhibits Esophageal Cancer by Downregulating NF-kappaB/COX-2/VEGF Pathway. Cisplatin 47-56 nuclear factor kappa B subunit 1 Homo sapiens 102-111 33813381-8 2021 RESULTS: Nuclear translocation of NF-kappaB in TE-1 cells was synergistically decreased by CDDP and EPA. Cisplatin 91-95 nuclear factor kappa B subunit 1 Homo sapiens 34-43 33813381-12 2021 CONCLUSION: The combination of CDDP and EPA synergistically suppresses NF-kappaB nuclear translocation and increases apoptosis by inducing cell cycle arrest at the S or G2/M phase. Cisplatin 31-35 nuclear factor kappa B subunit 1 Homo sapiens 71-80 33530952-10 2021 Furthermore, cisplatin treatment led to nuclear import of NFkappaB, which was diminished upon pre-treatment with INI-43. Cisplatin 13-22 nuclear factor kappa B subunit 1 Homo sapiens 58-66 33392640-1 2021 OBJECTIVE: To investigate the effects of FSTL1-mediated NF-kappaB signaling pathway on cisplatin (DDP) sensitivity of EOC cells. Cisplatin 87-96 nuclear factor kappa B subunit 1 Homo sapiens 56-65 33392640-1 2021 OBJECTIVE: To investigate the effects of FSTL1-mediated NF-kappaB signaling pathway on cisplatin (DDP) sensitivity of EOC cells. Cisplatin 98-101 nuclear factor kappa B subunit 1 Homo sapiens 56-65 33423764-15 2021 Therefore, we conclude that NF-kappaB pathway and IFNbeta pathway residing in the downstream of STING are resposible for apoptosis of UVB-irradiated or cisplatin-treated HaCaT cells. Cisplatin 152-161 nuclear factor kappa B subunit 1 Homo sapiens 28-37 33738336-0 2021 PTOV1 promotes cisplatin-induced chemotherapy resistance by activating the nuclear factor kappa B pathway in ovarian cancer. Cisplatin 15-24 nuclear factor kappa B subunit 1 Homo sapiens 75-97 33738336-6 2021 Inhibition of the NF-kappaB pathway in PTOV1-overexpressing ovarian cancer cells increased CDDP-induced apoptosis, suggesting that PTOV1 promoted chemotherapy resistance by activating the NF-kappaB pathway. Cisplatin 91-95 nuclear factor kappa B subunit 1 Homo sapiens 18-27 33738336-6 2021 Inhibition of the NF-kappaB pathway in PTOV1-overexpressing ovarian cancer cells increased CDDP-induced apoptosis, suggesting that PTOV1 promoted chemotherapy resistance by activating the NF-kappaB pathway. Cisplatin 91-95 nuclear factor kappa B subunit 1 Homo sapiens 188-197 33530952-11 2021 NFkappaB reporter activity and expression of NFkappaB transcriptional targets, cyclin D1, c-Myc and XIAP, showed decreased levels after combination treatment compared to single cisplatin treatment and this associated with enhanced DNA damage. Cisplatin 177-186 nuclear factor kappa B subunit 1 Homo sapiens 0-8 33530952-11 2021 NFkappaB reporter activity and expression of NFkappaB transcriptional targets, cyclin D1, c-Myc and XIAP, showed decreased levels after combination treatment compared to single cisplatin treatment and this associated with enhanced DNA damage. Cisplatin 177-186 nuclear factor kappa B subunit 1 Homo sapiens 45-53 33288565-5 2020 RESULTS: Both amentoflavone and QNZ (NF-kappaB inhibitor) significantly increased cisplatin-induced cytotoxicity. Cisplatin 82-91 nuclear factor kappa B subunit 1 Homo sapiens 37-46 32918990-0 2021 Kanglaite enhances the efficacy of cisplatin in suppression of hepatocellular carcinoma via inhibiting CKLF1 mediated NF-kappaB pathway and regulating transporter mediated drug efflux. Cisplatin 35-44 nuclear factor kappa B subunit 1 Homo sapiens 118-127 32918990-14 2021 Furthermore, CDDP activated NF-kappaBeta and promoted translocation of NF-kappaB toward the nucleus. Cisplatin 13-17 nuclear factor kappa B subunit 1 Homo sapiens 28-40 32918990-14 2021 Furthermore, CDDP activated NF-kappaBeta and promoted translocation of NF-kappaB toward the nucleus. Cisplatin 13-17 nuclear factor kappa B subunit 1 Homo sapiens 28-37 32918990-16 2021 Overexpression of CKLF1 reversed the effects of KLT on CDDP injured HepG2 cells, which exhibited by increased cell viability and enhanced activation of NF-kappaBeta. Cisplatin 55-59 nuclear factor kappa B subunit 1 Homo sapiens 152-164 32918990-17 2021 CDDP induced NF-kappaBeta activation could also lead to excessive inflammatory response, and KLT can suppress the aggravating inflammation which may be beneficial for tumor progression. Cisplatin 0-4 nuclear factor kappa B subunit 1 Homo sapiens 13-25 32918990-20 2021 The mechanisms may partly by inhibiting CKLF1 mediated NF-kappaB pathway, which may contribute to inflammation of tumor microenvironment and chemoresistance of CDDP. Cisplatin 160-164 nuclear factor kappa B subunit 1 Homo sapiens 55-64 32698736-6 2021 In addition, gossypin led to a significant increase in apoptosis genes (CASP3, CASP9) when compared to control while it caused a reduce in the level of NFKB1, which is accepted as apoptosis inhibitor (p< 0.05) (cisplatin-like). Cisplatin 211-220 nuclear factor kappa B subunit 1 Homo sapiens 152-157 33288565-1 2020 BACKGROUND/AIM: Nuclear factor kappa B (NF-kappaB) inactivation and apoptosis activation have been shown to enhance the anticancer effect of cisplatin in oral squamous cell carcinoma (OSCC). Cisplatin 141-150 nuclear factor kappa B subunit 1 Homo sapiens 16-38 33288565-1 2020 BACKGROUND/AIM: Nuclear factor kappa B (NF-kappaB) inactivation and apoptosis activation have been shown to enhance the anticancer effect of cisplatin in oral squamous cell carcinoma (OSCC). Cisplatin 141-150 nuclear factor kappa B subunit 1 Homo sapiens 40-49 33288565-6 2020 Amentoflavone reduced cisplatin-triggered NF-kappaB activity and enhanced cisplatin-induced intrinsic caspase-dependent and independent apoptotic pathways. Cisplatin 22-31 nuclear factor kappa B subunit 1 Homo sapiens 42-51 33288565-8 2020 CONCLUSION: Inactivation of NF-kappaB and induction of apoptosis through intrinsic caspase-dependent and independent apoptotic pathways are associated with amentoflavone enhanced anti-OSCC efficacy of cisplatin. Cisplatin 201-210 nuclear factor kappa B subunit 1 Homo sapiens 28-37 32945500-0 2020 Inactivation of AKT/NF-kappaB signaling by eurycomalactone decreases human NSCLC cell viability and improves the chemosensitivity to cisplatin. Cisplatin 133-142 nuclear factor kappa B subunit 1 Homo sapiens 20-29 32945500-10 2020 Exposure to cisplatin alone induced the levels of phosphorylated-AKT and phosphorylated-NF-kappaB, whereas co-treatment with ECL inhibited the cisplatin-induced phosphorylation of AKT and NF-kappaB, leading to an increased sensitization effect on cisplatin-induced apoptosis. Cisplatin 143-152 nuclear factor kappa B subunit 1 Homo sapiens 188-197 32945500-10 2020 Exposure to cisplatin alone induced the levels of phosphorylated-AKT and phosphorylated-NF-kappaB, whereas co-treatment with ECL inhibited the cisplatin-induced phosphorylation of AKT and NF-kappaB, leading to an increased sensitization effect on cisplatin-induced apoptosis. Cisplatin 143-152 nuclear factor kappa B subunit 1 Homo sapiens 188-197 33014864-0 2020 Combination of Tanshinone IIA and Cisplatin Inhibits Esophageal Cancer by Downregulating NF-kappaB/COX-2/VEGF Pathway. Cisplatin 34-43 nuclear factor kappa B subunit 1 Homo sapiens 89-98 32982420-0 2020 High Expression of Nuclear Transcription Factor-kappaB is Associated with Cisplatin Resistance and Prognosis for Ovarian Cancer. Cisplatin 74-83 nuclear factor kappa B subunit 1 Homo sapiens 19-54 32982420-10 2020 Western blotting showed that NF-kappaB p65 level in cisplatin-resistant cells (C13* and A2780cp) was significantly higher than that in cisplatin-sensitive cells (OV2008 and A2780s) (P < 0.05), and this increased expression could be suppressed by NF-kappaB inhibitor-PDTC treatment. Cisplatin 52-61 nuclear factor kappa B subunit 1 Homo sapiens 29-38 32982420-14 2020 The NF-kappaB inhibitor PDTC can enhance cisplatin sensitivity of platinum-resistant C13* and A2780cp ovarian cancer cells. Cisplatin 41-50 nuclear factor kappa B subunit 1 Homo sapiens 4-13 32559147-6 2020 Expert Opinion: microRNAs can positively or negatively regulate cisplatin resistance by acting on molecules or/and pathways related to apoptosis, autophagy, hypoxia, cancer stem cells, NF-kappaB and Notch1. Cisplatin 64-73 nuclear factor kappa B subunit 1 Homo sapiens 185-194 32945500-1 2020 The high activation of protein kinase B (AKT)/nuclear factor-kappaB (NF-kappaB) signaling has often been associated with the induction of non-small cell lung cancer (NSCLC) cell survival and resistance to cisplatin, which is one of the most widely used chemotherapeutic drugs in the treatment of NSCLC. Cisplatin 205-214 nuclear factor kappa B subunit 1 Homo sapiens 69-78 32945500-10 2020 Exposure to cisplatin alone induced the levels of phosphorylated-AKT and phosphorylated-NF-kappaB, whereas co-treatment with ECL inhibited the cisplatin-induced phosphorylation of AKT and NF-kappaB, leading to an increased sensitization effect on cisplatin-induced apoptosis. Cisplatin 12-21 nuclear factor kappa B subunit 1 Homo sapiens 88-97 32945500-10 2020 Exposure to cisplatin alone induced the levels of phosphorylated-AKT and phosphorylated-NF-kappaB, whereas co-treatment with ECL inhibited the cisplatin-induced phosphorylation of AKT and NF-kappaB, leading to an increased sensitization effect on cisplatin-induced apoptosis. Cisplatin 12-21 nuclear factor kappa B subunit 1 Homo sapiens 188-197 32567210-4 2020 Cisplatin-treated hNP cells exhibited rapid phosphorylation of ATM and subsequent increased NF-kappaB activation, aggrecanolysis, decreased total proteoglycan production and increased expression of markers of senescence, including p21, gammaH2 AX and SA-ss-gal. Cisplatin 0-9 nuclear factor kappa B subunit 1 Homo sapiens 92-101 32784919-7 2020 Molecularly, Western blot analysis revealed that CDDP strongly increased Akt and moderately reduced p-NF-kappaB and p-IkappaB and that AIMs inhibited CDDP-induced Akt activation, and augmented CDDP-induced reduction of p-NF-kappaB and p-IkappaB in MCF-7 cells. Cisplatin 49-53 nuclear factor kappa B subunit 1 Homo sapiens 102-111 32784919-7 2020 Molecularly, Western blot analysis revealed that CDDP strongly increased Akt and moderately reduced p-NF-kappaB and p-IkappaB and that AIMs inhibited CDDP-induced Akt activation, and augmented CDDP-induced reduction of p-NF-kappaB and p-IkappaB in MCF-7 cells. Cisplatin 150-154 nuclear factor kappa B subunit 1 Homo sapiens 221-230 32784919-7 2020 Molecularly, Western blot analysis revealed that CDDP strongly increased Akt and moderately reduced p-NF-kappaB and p-IkappaB and that AIMs inhibited CDDP-induced Akt activation, and augmented CDDP-induced reduction of p-NF-kappaB and p-IkappaB in MCF-7 cells. Cisplatin 150-154 nuclear factor kappa B subunit 1 Homo sapiens 221-230 32784919-10 2020 In conclusion, AIMs enhanced CDDP sensitivity by inhibiting Akt and NF-kappaB activity of MCF-7 cells that show relative intrinsic CDDP resistance. Cisplatin 29-33 nuclear factor kappa B subunit 1 Homo sapiens 68-77 32259551-0 2020 Crocin attenuates cisplatin-induced hepatotoxicity via TLR4/NF-kappaBp50 signaling and BAMBI modulation of TGF-beta activity: Involvement of miRNA-9 and miRNA-29. Cisplatin 18-27 nuclear factor kappa B subunit 1 Homo sapiens 60-72 31974389-6 2020 Curcumin exerts permissive and chemosensitive properties by targeting the cisplatin chemoresistant factors Nrf-2, NF-kappaB and STAT-3 phosphorylation. Cisplatin 74-83 nuclear factor kappa B subunit 1 Homo sapiens 114-123 32141535-10 2020 CONCLUSIONS: Targeting microRNA1301 can inhibit the proliferation of cisplatin-resistant cells and the development of EMT in human ovarian cancer cells by inhibiting the NF-kappaB signaling pathway, thereby inhibiting the occurrence and development of drug-resistant ovarian cancer. Cisplatin 69-78 nuclear factor kappa B subunit 1 Homo sapiens 170-179 31905343-7 2020 In addition, we demonstrated that the enhanced effect of aspirin on the cisplatin-induced inhibition of tumor cell growth was also mediated through the suppression of the binding activity of NF-kappaB to the COX-2 promoter. Cisplatin 72-81 nuclear factor kappa B subunit 1 Homo sapiens 191-200 31905343-8 2020 The combination of aspirin and cisplatin effectively attenuated the translocation of NF-kappaB p65/p50 from the cytoplasm to the nucleus, and abrogated the binding of NF-kappaB p65/p50 to the COX-2 promoter, thereby down-regulating COX-2 expression and PGE2 synthesis. Cisplatin 31-40 nuclear factor kappa B subunit 1 Homo sapiens 99-102 31905343-8 2020 The combination of aspirin and cisplatin effectively attenuated the translocation of NF-kappaB p65/p50 from the cytoplasm to the nucleus, and abrogated the binding of NF-kappaB p65/p50 to the COX-2 promoter, thereby down-regulating COX-2 expression and PGE2 synthesis. Cisplatin 31-40 nuclear factor kappa B subunit 1 Homo sapiens 181-184 32428872-5 2020 High phosphoinositide 3-kinase (PI3K), Akt and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) phosphorylation levels were observed in cisplatin-resistant cells. Cisplatin 162-171 nuclear factor kappa B subunit 1 Homo sapiens 111-120 32428872-6 2020 Pretreating chondrosarcoma cells with PI3K, Akt and NF-kappaB inhibitors or transfecting the cells with p85, Akt and p65 siRNAs potentiated cisplatin-induced cytotoxicity. Cisplatin 140-149 nuclear factor kappa B subunit 1 Homo sapiens 52-61 32435511-0 2020 Inhibition of IKKbeta/NF-kappaB signaling pathway to improve Dasatinib efficacy in suppression of cisplatin-resistant head and neck squamous cell carcinoma. Cisplatin 98-107 nuclear factor kappa B subunit 1 Homo sapiens 22-31 32435511-4 2020 In this study, we investigated the role of IKKbeta/NF-kappaB in regulation of the sensitivity of cisplatin-resistant HNSCC to Dasatinib. Cisplatin 97-106 nuclear factor kappa B subunit 1 Homo sapiens 51-60 32435511-5 2020 Additionally, we wished to determine whether inhibition of the IKKbeta/NF-kappaB signaling pathway could enhance Dasatinib efficacy to inhibit cisplatin-resistant HNSCC without the use of cisplatin. Cisplatin 143-152 nuclear factor kappa B subunit 1 Homo sapiens 71-80 32435511-7 2020 We found that SRC kinase inhibition by Dasatinib decreased ETS-1 expression but caused elevation of IKKbeta/NF-kappaB signaling in multiple cisplatin-resistant HNSCC. Cisplatin 140-149 nuclear factor kappa B subunit 1 Homo sapiens 108-117 32509178-0 2020 MARK2 enhances cisplatin resistance via PI3K/AKT/NF-kappaB signaling pathway in osteosarcoma cells. Cisplatin 15-24 nuclear factor kappa B subunit 1 Homo sapiens 49-58 32509178-8 2020 Mechanistically, MARK2 overexpression enhanced P-glycoprotein expression and decreased cell apoptosis through PI3K/AKT/NF-kappaB signaling pathway activation, resulting in cisplatin resistance. Cisplatin 172-181 nuclear factor kappa B subunit 1 Homo sapiens 119-128 32328193-0 2020 Self-enforcing HMGB1/NF-kappaB/HIF-1alpha Feedback Loop Promotes Cisplatin Resistance in Hepatocellular Carcinoma Cells. Cisplatin 65-74 nuclear factor kappa B subunit 1 Homo sapiens 21-30 32328193-6 2020 Further, we showed that HMGB1 has an important role in mediating cisplatin resistance via an HMGB1/ nuclear factor kappa-B (NF-kappaB)/ hypoxia inducible factor-1alpha (HIF-1alpha) feedback loop. Cisplatin 65-74 nuclear factor kappa B subunit 1 Homo sapiens 100-122 32328193-6 2020 Further, we showed that HMGB1 has an important role in mediating cisplatin resistance via an HMGB1/ nuclear factor kappa-B (NF-kappaB)/ hypoxia inducible factor-1alpha (HIF-1alpha) feedback loop. Cisplatin 65-74 nuclear factor kappa B subunit 1 Homo sapiens 124-133 31905343-0 2020 Aspirin enhances the sensitivity of colon cancer cells to cisplatin by abrogating the binding of NF-kappaB to the COX-2 promoter. Cisplatin 58-67 nuclear factor kappa B subunit 1 Homo sapiens 97-106 31790894-16 2020 The combination of CDDP/PXD and TK or CuD inhibited p-AKT, p-Erk, and p-JNK signaling and suppressed Stat3 and NF-kappaB transcriptional activity in H1299 cells. Cisplatin 19-23 nuclear factor kappa B subunit 1 Homo sapiens 111-120 31497913-0 2020 Quercetin protects against cisplatin-induced acute kidney injury by inhibiting Mincle/Syk/NF-kappaB signaling maintained macrophage inflammation. Cisplatin 27-36 nuclear factor kappa B subunit 1 Homo sapiens 90-99 31895687-9 2019 Ubenimex inhibits the activation of the CD13/EMP3/PI3K/AKT/NF-kappaB pathway to overcome CDDP resistance in GC cells by suppressing autophagy and epithelial-mesenchymal transition (EMT). Cisplatin 89-93 nuclear factor kappa B subunit 1 Homo sapiens 59-68 31818359-9 2019 We also investigated NF-kappaB, the upstream regulator of EMT markers, and discovered that Cis-DDP treatment led to NF-kappaB translocation in the nucleus as well as its promoter activity. Cisplatin 91-98 nuclear factor kappa B subunit 1 Homo sapiens 21-30 31819048-0 2019 Vitamin D promotes the cisplatin sensitivity of oral squamous cell carcinoma by inhibiting LCN2-modulated NF-kappaB pathway activation through RPS3. Cisplatin 23-32 nuclear factor kappa B subunit 1 Homo sapiens 106-115 31818359-9 2019 We also investigated NF-kappaB, the upstream regulator of EMT markers, and discovered that Cis-DDP treatment led to NF-kappaB translocation in the nucleus as well as its promoter activity. Cisplatin 91-98 nuclear factor kappa B subunit 1 Homo sapiens 116-125 31518663-5 2019 Mechanistically, cisplatin induced PTGS2 expression through ROS/NF-kappaB pathway. Cisplatin 17-26 nuclear factor kappa B subunit 1 Homo sapiens 64-73 31037726-5 2019 c-Myb overexpression activated NF-kappaB and STAT3 signaling leading to enhanced proliferation, invasion, and cisplatin resistance. Cisplatin 110-119 nuclear factor kappa B subunit 1 Homo sapiens 31-40 31446998-0 2019 Targeting NF-kappaB-mediated inflammatory pathways in cisplatin-resistant NSCLC. Cisplatin 54-63 nuclear factor kappa B subunit 1 Homo sapiens 10-19 31364751-11 2019 Therefore, the present results suggested that SOD-2 may serve as an oncogene, and the upregulation of SOD-2 by TNF-alpha/NF-kappaB may contribute to cisplatin resistance in ESCC. Cisplatin 149-158 nuclear factor kappa B subunit 1 Homo sapiens 121-130 31446998-7 2019 The cisplatin sensitizing potential of an NF-kappaB small molecule inhibitor, DHMEQ, was also assessed by means of viability assays and western blot analysis. Cisplatin 4-13 nuclear factor kappa B subunit 1 Homo sapiens 42-51 31446998-9 2019 DHMEQ treatment resulted in reduced NF-kappaB expression in the presence of cisplatin, and re-sensitized CisR cells to the cytotoxic effects of the drug. Cisplatin 76-85 nuclear factor kappa B subunit 1 Homo sapiens 36-45 30718500-0 2019 CHD1L contributes to cisplatin resistance by upregulating the ABCB1-NF-kappaB axis in human non-small-cell lung cancer. Cisplatin 21-30 nuclear factor kappa B subunit 1 Homo sapiens 68-77 30631898-2 2019 Since metastasis-associated protein 1 (MTA1) upregulation and augmentation of APOBEC3B expression are both strongly associated with cervical cancer (CCa) development, and both molecules have been shown to be functionally associated with NF-kappaB pathway, we therefore sought to investigate the potential mechanistic link between MTA1, APOBEC3B and NF-kappaB during the pathogenesis of cisplatin (CDDP) resistance in HPV-positive CCa cells. Cisplatin 386-395 nuclear factor kappa B subunit 1 Homo sapiens 237-246 30631898-2 2019 Since metastasis-associated protein 1 (MTA1) upregulation and augmentation of APOBEC3B expression are both strongly associated with cervical cancer (CCa) development, and both molecules have been shown to be functionally associated with NF-kappaB pathway, we therefore sought to investigate the potential mechanistic link between MTA1, APOBEC3B and NF-kappaB during the pathogenesis of cisplatin (CDDP) resistance in HPV-positive CCa cells. Cisplatin 397-401 nuclear factor kappa B subunit 1 Homo sapiens 237-246 30631898-11 2019 CONCLUSIONS: These findings reveal an obligatory coregulatory role of MTA1 in the indirect regulation of APOBEC3B expression via classical NF-kappaB pathway, and also suggest that inhibition of MTA1/NF-kappaB/APOBEC3B cascade may be repositioned to suppress cancer mutagenesis, dampen tumor evolution, and decrease the probability of adverse outcomes from CDDP resistance in CCa. Cisplatin 356-360 nuclear factor kappa B subunit 1 Homo sapiens 199-208 29572052-10 2018 Inhibiting AXL/PI3K/Akt/NF-kappaB signaling pathway reversed the effects of DANCR on cisplatin resistance. Cisplatin 85-94 nuclear factor kappa B subunit 1 Homo sapiens 24-33 30508513-0 2019 NFkappaB and TNFalpha as individual key molecules associated with the cisplatin-resistance and radioresistance of lung cancer. Cisplatin 70-79 nuclear factor kappa B subunit 1 Homo sapiens 0-8 30508513-4 2019 In qPCR analyses of screening DNA repair and cell survival-associated molecules, we identified NFkappaB and TNFalpha as the most significantly up-regulated molecules in cisplatin-resistant and radioresistant lung cancer cells, respectively, compared with parental cells. Cisplatin 169-178 nuclear factor kappa B subunit 1 Homo sapiens 95-103 30564368-0 2019 MDM2 inhibitor ameliorates cisplatin-induced nephropathy via NFkappaBeta signal inhibition. Cisplatin 27-36 nuclear factor kappa B subunit 1 Homo sapiens 61-72 30564368-4 2019 However, independent of p53, MDM2 acts as a co-transcription factor for nuclear factor-kappaB (NFkappaB), whose signaling can be involved in cisplatin-induced tubular injury. Cisplatin 141-150 nuclear factor kappa B subunit 1 Homo sapiens 72-93 30564368-4 2019 However, independent of p53, MDM2 acts as a co-transcription factor for nuclear factor-kappaB (NFkappaB), whose signaling can be involved in cisplatin-induced tubular injury. Cisplatin 141-150 nuclear factor kappa B subunit 1 Homo sapiens 95-103 30564368-9 2019 Western blotting showed that cisplatin increased NFkappaB phosphorylation in kidneys, which was significantly suppressed by DS-5272. Cisplatin 29-38 nuclear factor kappa B subunit 1 Homo sapiens 49-57 30564368-12 2019 Collectively, these findings suggest that DS-5272 can ameliorate cisplatin nephrotoxicity via NFkappaB signal inhibition. Cisplatin 65-74 nuclear factor kappa B subunit 1 Homo sapiens 94-102 30274235-5 2018 Finally, FHC knock-down in K562 and SKOV3 cancer cell lines resulted in an improved cell viability following doxorubicin or cisplatin treatment, being counteracted by the transient expression of inhibitory of NF-kappaB, IkappaBalpha. Cisplatin 124-133 nuclear factor kappa B subunit 1 Homo sapiens 209-218 30464531-15 2018 Conclusion: Taken together, our results indicated that TRIM32 is overexpressed in NSCLC and regulates cisplatin resistance, possibly through NF-kappaB and Bcl-2. Cisplatin 102-111 nuclear factor kappa B subunit 1 Homo sapiens 141-150 29572052-0 2018 Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-kappaB signaling pathway. Cisplatin 34-43 nuclear factor kappa B subunit 1 Homo sapiens 99-108 29572052-12 2018 DANCR promotes cisplatin resistance via activating AXL/PI3K/Akt/NF-kappaB signaling pathway in glioma. Cisplatin 15-24 nuclear factor kappa B subunit 1 Homo sapiens 64-73 30104883-0 2018 Combination chemotherapy with Zyflamend reduced the acquired resistance of bladder cancer cells to cisplatin through inhibiting NFkappaB signaling pathway. Cisplatin 99-108 nuclear factor kappa B subunit 1 Homo sapiens 128-136 30104883-10 2018 Results: Comparing to that in the parental T24 cells, NFkappaB is constitutively active in cisplatin-resistant T24R cells. Cisplatin 91-100 nuclear factor kappa B subunit 1 Homo sapiens 54-62 29950928-0 2018 ETS1 is associated with cisplatin resistance through IKKalpha/NF-kappaB pathway in cell line MDA-MB-231. Cisplatin 24-33 nuclear factor kappa B subunit 1 Homo sapiens 62-71 29386467-10 2018 Cisplatin stimulated protein kinase B (Akt) and nuclear factor-kappaB (NF-kappaB) signaling pathways, but not mitogen-activated protein kinase (MAPK), activator protein 1 (AP-1) and signal transducer and activator of transcription 3 (STAT3) in SKOV3 cells. Cisplatin 0-9 nuclear factor kappa B subunit 1 Homo sapiens 48-69 29524521-12 2018 We suggest that CLDN1 is upregulated by CDDP resistance through activation of a PI3K/Akt/NF-kappaB pathway, resulting in the inhibition of penetration of anticancer drugs into the inner area of spheroids. Cisplatin 40-44 nuclear factor kappa B subunit 1 Homo sapiens 89-98 29393335-8 2018 In conclusion, SchB regulates ERK/NF-kappaB signaling to induce the expression of survivin, thereby alleviating cis-DDP-induced renal injury. Cisplatin 112-119 nuclear factor kappa B subunit 1 Homo sapiens 34-43 29567488-4 2018 In this study, we showed that activation of nuclear factor-kappaB (NF-kappaB) is significantly higher in therapy-resistant EOC cells compared to chemosensitive counterparts, which was positively associated with resistance to cisplatin, carboplatin, paclitaxel and erlotinib. Cisplatin 225-234 nuclear factor kappa B subunit 1 Homo sapiens 44-65 29567488-4 2018 In this study, we showed that activation of nuclear factor-kappaB (NF-kappaB) is significantly higher in therapy-resistant EOC cells compared to chemosensitive counterparts, which was positively associated with resistance to cisplatin, carboplatin, paclitaxel and erlotinib. Cisplatin 225-234 nuclear factor kappa B subunit 1 Homo sapiens 67-76 29743526-4 2018 It was further shown that HQH administration reduced cisplatin-induced release and nuclear-cytoplasmic translocation of HMGB1 and inactivated its downstream signaling molecules, TLR4 and NFkappaB, in renal tubular cells; as a result, HQH repressed cisplatin-induced TNF-alpha production. Cisplatin 53-62 nuclear factor kappa B subunit 1 Homo sapiens 187-195 29393335-0 2018 Schizandrin B inhibits the cis-DDP-induced apoptosis of HK-2 cells by activating ERK/NF-kappaB signaling to regulate the expression of survivin. Cisplatin 27-34 nuclear factor kappa B subunit 1 Homo sapiens 85-94 29386467-10 2018 Cisplatin stimulated protein kinase B (Akt) and nuclear factor-kappaB (NF-kappaB) signaling pathways, but not mitogen-activated protein kinase (MAPK), activator protein 1 (AP-1) and signal transducer and activator of transcription 3 (STAT3) in SKOV3 cells. Cisplatin 0-9 nuclear factor kappa B subunit 1 Homo sapiens 71-80 29386467-11 2018 Akt/NF-kappaB signaling was blocked by CN and OMBC leading to increased sensitization to cisplatin. Cisplatin 89-98 nuclear factor kappa B subunit 1 Homo sapiens 4-13 29386467-12 2018 These findings demonstrate that CN and OMBC sensitizes SKOV3 cells to cisplatin via inhibition of Akt/NF-kappaB signaling and the down regulation of NF-kappaB mediated gene products. Cisplatin 70-79 nuclear factor kappa B subunit 1 Homo sapiens 102-111 29386467-12 2018 These findings demonstrate that CN and OMBC sensitizes SKOV3 cells to cisplatin via inhibition of Akt/NF-kappaB signaling and the down regulation of NF-kappaB mediated gene products. Cisplatin 70-79 nuclear factor kappa B subunit 1 Homo sapiens 149-158 28518145-3 2017 In this study, we sought to investigate the role of cytoplasmic RAP1, a previously identified positive regulator of NF-kappaB signaling, in the development of cisplatin resistance in NSCLC cells. Cisplatin 159-168 nuclear factor kappa B subunit 1 Homo sapiens 116-125 29228621-0 2017 Synergism of ursolic acid and cisplatin promotes apoptosis and enhances growth inhibition of cervical cancer cells via suppressing NF-kappaB p65. Cisplatin 30-39 nuclear factor kappa B subunit 1 Homo sapiens 131-140 28498503-0 2017 p62/SQSTM1 as an oncotarget mediates cisplatin resistance through activating RIP1-NF-kappaB pathway in human ovarian cancer cells. Cisplatin 37-46 nuclear factor kappa B subunit 1 Homo sapiens 82-91 28498503-6 2017 In this study, we demonstrate that the activity of the NF-kappaB signaling pathway and K63-linked ubiquitination of RIP1 was higher in cisplatin-resistant ovarian (SKOV3/DDP) cells compared with parental cells. Cisplatin 135-144 nuclear factor kappa B subunit 1 Homo sapiens 55-64 28978336-0 2017 The oncogenic Golgi phosphoprotein 3 like overexpression is associated with cisplatin resistance in ovarian carcinoma and activating the NF-kappaB signaling pathway. Cisplatin 76-85 nuclear factor kappa B subunit 1 Homo sapiens 137-146 28415048-0 2017 Baicalein increases cisplatin sensitivity of A549 lung adenocarcinoma cells via PI3K/Akt/NF-kappaB pathway. Cisplatin 20-29 nuclear factor kappa B subunit 1 Homo sapiens 89-98 28415048-4 2017 We found that A549/CDDP (resistant to CDDP) cells not only acquired epithelial-mesenchymal transition (EMT) phenotype, but also showed increased NF-kappaB activity compared with A549 cells (sensitive to CDDP). Cisplatin 19-23 nuclear factor kappa B subunit 1 Homo sapiens 145-154 28415048-4 2017 We found that A549/CDDP (resistant to CDDP) cells not only acquired epithelial-mesenchymal transition (EMT) phenotype, but also showed increased NF-kappaB activity compared with A549 cells (sensitive to CDDP). Cisplatin 38-42 nuclear factor kappa B subunit 1 Homo sapiens 145-154 28415048-4 2017 We found that A549/CDDP (resistant to CDDP) cells not only acquired epithelial-mesenchymal transition (EMT) phenotype, but also showed increased NF-kappaB activity compared with A549 cells (sensitive to CDDP). Cisplatin 38-42 nuclear factor kappa B subunit 1 Homo sapiens 145-154 28415048-5 2017 Our study further demonstrated that PI3K/Akt/NF-kappaB pathway controlled CDDP resistance via EMT and NF-kappaB-mediated apoptosis. Cisplatin 74-78 nuclear factor kappa B subunit 1 Homo sapiens 45-54 28415048-5 2017 Our study further demonstrated that PI3K/Akt/NF-kappaB pathway controlled CDDP resistance via EMT and NF-kappaB-mediated apoptosis. Cisplatin 74-78 nuclear factor kappa B subunit 1 Homo sapiens 102-111 28518145-5 2017 The RAP1-mediated cisplatin resistance was associated with the activation of NF-kappaB signaling and the upregulation of the antiapoptosis factor BCL-2. Cisplatin 18-27 nuclear factor kappa B subunit 1 Homo sapiens 77-86 28518145-8 2017 Hence, our results demonstrate that the cytoplasmic RAP1-NF-kappaB-BCL2 axis represents a key pathway to cisplatin resistance in NSCLC cells, identifying RAP1 as a marker and a potential therapeutic target for cisplatin resistance of NSCLC. Cisplatin 105-114 nuclear factor kappa B subunit 1 Homo sapiens 57-66 28518145-8 2017 Hence, our results demonstrate that the cytoplasmic RAP1-NF-kappaB-BCL2 axis represents a key pathway to cisplatin resistance in NSCLC cells, identifying RAP1 as a marker and a potential therapeutic target for cisplatin resistance of NSCLC. Cisplatin 210-219 nuclear factor kappa B subunit 1 Homo sapiens 57-66 27995416-12 2017 The cancer cells treated by echistatin, cisplatin, and in particular the combination of both compounds drastically increased expression of NFkappaB transcription factor. Cisplatin 40-49 nuclear factor kappa B subunit 1 Homo sapiens 139-147 28400607-6 2017 Etoposide and cisplatin increased NFkappaB promoter reporter activity and etoposide induced nuclear translocation of NFkappaB. Cisplatin 14-23 nuclear factor kappa B subunit 1 Homo sapiens 34-42 28400607-10 2017 These data demonstrate for the first time that etoposide- and cisplatin-induced apoptosis in medulloblastoma and glioblastoma cell lines is mediated in part by PID1, involves NFkappaB, and may be regulated by proteasomal degradation. Cisplatin 62-71 nuclear factor kappa B subunit 1 Homo sapiens 175-183 28119452-8 2017 Blockade of P53 or NF-kappaB attenuated cisplatin-induced miR-375 expression, supporting a role of P53 and NF-kappaB in miR-375 induction. Cisplatin 40-49 nuclear factor kappa B subunit 1 Homo sapiens 19-28 28119452-8 2017 Blockade of P53 or NF-kappaB attenuated cisplatin-induced miR-375 expression, supporting a role of P53 and NF-kappaB in miR-375 induction. Cisplatin 40-49 nuclear factor kappa B subunit 1 Homo sapiens 107-116 28119452-11 2017 Together, these results suggest that upon cisplatin exposure, P53 and NF-kappaB collaboratively induce miR-375 expression, which, in turn, represses HNF-1beta activity, resulting in renal tubular cell apoptosis and nephrotoxicity. Cisplatin 42-51 nuclear factor kappa B subunit 1 Homo sapiens 70-79 27754745-6 2017 Cisplatin-resistant osteosarcoma cells showed NFKB1/NFkappaB-mediated GFRA1 expression. Cisplatin 0-9 nuclear factor kappa B subunit 1 Homo sapiens 46-51 28182789-9 2017 Western blot results demonstrated that cisplatin increased TLR4 and NF-kappaB protein expression in the kidney tissues. Cisplatin 39-48 nuclear factor kappa B subunit 1 Homo sapiens 68-77 28182789-12 2017 The promotion effects might be attributed to suppression of cisplatin-increased NF-kappaB p65 expression by puerarin. Cisplatin 60-69 nuclear factor kappa B subunit 1 Homo sapiens 80-89 28255357-0 2017 STAT3/NF-kappaB-Regulated Lentiviral TK/GCV Suicide Gene Therapy for Cisplatin-Resistant Triple-Negative Breast Cancer. Cisplatin 69-78 nuclear factor kappa B subunit 1 Homo sapiens 6-15 28255357-14 2017 Moreover, STAT3/NF-kappaB signaling targeting could further sensitize tumor cells to cisplatin. Cisplatin 85-94 nuclear factor kappa B subunit 1 Homo sapiens 16-25 27754745-6 2017 Cisplatin-resistant osteosarcoma cells showed NFKB1/NFkappaB-mediated GFRA1 expression. Cisplatin 0-9 nuclear factor kappa B subunit 1 Homo sapiens 52-60 26782341-5 2016 Pre-processing 1,25D3 inhibited expression of NF-kappaB/GPX1/uPA, which subsequently suppressed cell motility and cisplatin-resistance in ACC-2 cells. Cisplatin 114-123 nuclear factor kappa B subunit 1 Homo sapiens 46-55 27322140-7 2016 In these AR-positive cells, R1881 treatment also induced the expression levels of NF-kappaB, which is known to involve CDDP resistance, and its phosphorylated form, as well as nuclear translocation of NF-kappaB. Cisplatin 119-123 nuclear factor kappa B subunit 1 Homo sapiens 82-91 27322140-8 2016 In CDDP-resistant bladder cancer sublines established following long-term culture with CDDP, the expression levels of AR as well as NF-kappaB and phospho-NF-kappaB were considerably elevated, compared with respective control sublines. Cisplatin 3-7 nuclear factor kappa B subunit 1 Homo sapiens 132-141 27322140-8 2016 In CDDP-resistant bladder cancer sublines established following long-term culture with CDDP, the expression levels of AR as well as NF-kappaB and phospho-NF-kappaB were considerably elevated, compared with respective control sublines. Cisplatin 3-7 nuclear factor kappa B subunit 1 Homo sapiens 154-163 27322140-8 2016 In CDDP-resistant bladder cancer sublines established following long-term culture with CDDP, the expression levels of AR as well as NF-kappaB and phospho-NF-kappaB were considerably elevated, compared with respective control sublines. Cisplatin 87-91 nuclear factor kappa B subunit 1 Homo sapiens 132-141 27322140-8 2016 In CDDP-resistant bladder cancer sublines established following long-term culture with CDDP, the expression levels of AR as well as NF-kappaB and phospho-NF-kappaB were considerably elevated, compared with respective control sublines. Cisplatin 87-91 nuclear factor kappa B subunit 1 Homo sapiens 154-163 27322140-10 2016 These results suggest that AR activation correlates with CDDP resistance presumably via modulating NF-kappaB activity in bladder cancer cells. Cisplatin 57-61 nuclear factor kappa B subunit 1 Homo sapiens 99-108 27470347-0 2016 Interferon beta improves the efficacy of low dose cisplatin by inhibiting NF-kappaB/p-Akt signaling on HeLa cells. Cisplatin 50-59 nuclear factor kappa B subunit 1 Homo sapiens 74-83 27470347-6 2016 Results demonstrate that the synergistic inhibitory effects of interferon beta and low dose of cisplatin on human cervical cancer cells and also suggest that the inhibition of NF-kappaB/p-Akt signaling pathway plays a critical role in the anticancer effects of combination treatment along with the induction of PARP. Cisplatin 95-104 nuclear factor kappa B subunit 1 Homo sapiens 176-185 28123844-0 2017 Targeting NF-kappaB/AP-2beta signaling to enhance antitumor activity of cisplatin by melatonin in hepatocellular carcinoma cells. Cisplatin 72-81 nuclear factor kappa B subunit 1 Homo sapiens 10-19 28123844-6 2017 Further mechanism studies showed that the combined treatment of melatonin and cisplatin enhanced the cleavage of caspase-3, caspase-9 and poly-(ADP-ribose) polymerase (PARP), decreased the expression of Bcl-2 and p-IKKalpha/beta, suppressed the nuclear translocation of NF-kappaB p50/p65 proteins, and abrogated the binding of p65 to COX-2 promoter, thereby inhibiting COX-2 expression. Cisplatin 78-87 nuclear factor kappa B subunit 1 Homo sapiens 270-283 28123844-9 2017 Collectively, our results demonstrated that melatonin sensitizes the cisplatin-mediated growth suppression of cells via the inactivation of NF-kappaB/COX-2 and AP-2beta/hTERT signaling in hepatocellular carcinoma cells. Cisplatin 69-78 nuclear factor kappa B subunit 1 Homo sapiens 140-149 26704389-0 2016 Inhibition of nuclear factor kappaB transcription activity drives a synergistic effect of cisplatin and oridonin on HepG2 human hepatocellular carcinoma cells. Cisplatin 90-99 nuclear factor kappa B subunit 1 Homo sapiens 29-35 26704389-1 2016 Activation of nuclear factor kappaB (NF-kappaB) by cisplatin and other chemotherapeutics is responsible, at least in part, for the development of drug resistance in the treatment of hepatocellular carcinoma. Cisplatin 51-60 nuclear factor kappa B subunit 1 Homo sapiens 29-35 26704389-1 2016 Activation of nuclear factor kappaB (NF-kappaB) by cisplatin and other chemotherapeutics is responsible, at least in part, for the development of drug resistance in the treatment of hepatocellular carcinoma. Cisplatin 51-60 nuclear factor kappa B subunit 1 Homo sapiens 37-46 26673543-5 2016 The suppression of NF-kappaB activity following pioglitazone treatment inhibited the cisplatin-induced IkappaB-alpha degredation and NF-kappaB p65 subunit translocation. Cisplatin 85-94 nuclear factor kappa B subunit 1 Homo sapiens 133-142 26476534-8 2016 Moreover, it showed that downregulation of TAB3 enhanced CDDP-induced A549 cell apoptosis through the inhibition of the NF-kappaB pathway. Cisplatin 57-61 nuclear factor kappa B subunit 1 Homo sapiens 120-129 26673543-0 2016 The peroxisome proliferator-activated receptor gamma agonist pioglitazone prevents NF-kappaB activation in cisplatin nephrotoxicity through the reduction of p65 acetylation via the AMPK-SIRT1/p300 pathway. Cisplatin 107-116 nuclear factor kappa B subunit 1 Homo sapiens 83-92 26673543-3 2016 The aim of the present study was to evaluate whether the activation of PPAR-gamma attenuates the cisplatin-induced NF-kappaB activation in cisplatin nephrotoxicity. Cisplatin 97-106 nuclear factor kappa B subunit 1 Homo sapiens 115-124 26673543-3 2016 The aim of the present study was to evaluate whether the activation of PPAR-gamma attenuates the cisplatin-induced NF-kappaB activation in cisplatin nephrotoxicity. Cisplatin 139-148 nuclear factor kappa B subunit 1 Homo sapiens 115-124 26673543-4 2016 The results showed that the PPAR-gamma agonist pioglitazone decreased the expression of NF-kappaB p65 transcription target genes (e.g., IL-6, IL-1beta, and TNF-alpha) and inhibited histological injury and inflammatory cells infiltration in cisplatin nephrotoxicity. Cisplatin 240-249 nuclear factor kappa B subunit 1 Homo sapiens 88-97 26673543-5 2016 The suppression of NF-kappaB activity following pioglitazone treatment inhibited the cisplatin-induced IkappaB-alpha degredation and NF-kappaB p65 subunit translocation. Cisplatin 85-94 nuclear factor kappa B subunit 1 Homo sapiens 19-28 26673543-9 2016 These results suggest that the PPAR-gamma agonist pioglitazone prevents NF-kappaB activation in cisplatin nephrotoxicity through a reduction in p65 acetylation via the AMPK-SIRT1/p300 pathway. Cisplatin 96-105 nuclear factor kappa B subunit 1 Homo sapiens 72-81 26503358-0 2015 Caveolin-1 mediates chemoresistance in cisplatin-resistant ovarian cancer cells by targeting apoptosis through the Notch-1/Akt/NF-kappaB pathway. Cisplatin 39-48 nuclear factor kappa B subunit 1 Homo sapiens 127-136 26722370-0 2016 Triple-Layered pH-Responsive Micelleplexes Loaded with siRNA and Cisplatin Prodrug for NF-Kappa B Targeted Treatment of Metastatic Breast Cancer. Cisplatin 65-74 nuclear factor kappa B subunit 1 Homo sapiens 87-97 26722370-3 2016 We herein report a novel triple-layered pH-responsive micelleplex loading siRNA and alkylated cisplatin prodrug for NF-Kappa B targeted treatment of metastatic breast cancer. Cisplatin 94-103 nuclear factor kappa B subunit 1 Homo sapiens 116-126 26722370-8 2016 Using a 4T1 breast cancer model, we demonstrate that this novel micelleplex co-loaded with cisplatin prodrug and siRNA-p65 is able to simultaneously inhibit tumor growth and suppress distant metastasis of the cancer cells by downregulating NF-kappa B expression. Cisplatin 91-100 nuclear factor kappa B subunit 1 Homo sapiens 240-250 26503358-10 2015 Furthermore, knockdown of Cav-1 was also able to significantly downregulate the protein expression level of Notch-1, p-Akt and p-NF-kappaB p65 in cisplatin-resistant ovarian cancer cells. Cisplatin 146-155 nuclear factor kappa B subunit 1 Homo sapiens 129-138 26693062-0 2015 IKK phosphorylation of NF-kappaB at serine 536 contributes to acquired cisplatin resistance in head and neck squamous cell cancer. Cisplatin 71-80 nuclear factor kappa B subunit 1 Homo sapiens 23-32 26693062-8 2015 Additionally, the novel IKKbeta inhibitor CmpdA has been shown to consistently block the phosphorylation of NF-kappaB at serine 536 while also dramatically improving the efficacy of cisplatin in inhibition of cell proliferation and induction of apoptosis in the cisplatin resistant cancer cells. Cisplatin 262-271 nuclear factor kappa B subunit 1 Homo sapiens 108-117 26079730-5 2015 In vitro, knockdown of Eag1 by small interfering RNA facilitated the sensitivity of ovarian cancer cells (SKOV3 and TYK) to cisplatin-induced apoptosis via nuclear factor kappa-light chain-enhancer of activated B cells (NF-kappaB) pathway. Cisplatin 124-133 nuclear factor kappa B subunit 1 Homo sapiens 220-229 26498527-5 2015 Furthermore, a decrease in SIRT1 activity was found to play an important role in cisplatin-mediated small intestinal damage through nuclear factor (NF)-kappaB p65 activation, facilitated by its acetylation increase. Cisplatin 81-90 nuclear factor kappa B subunit 1 Homo sapiens 132-158 26498527-6 2015 However, use of dunnione as a strong substrate for the NADH:quinone oxidoreductase 1 (NQO1) enzyme led to an increase in intracellular NAD(+) levels and prevented the cisplatin-induced small intestinal damage correlating with the modulation of PARP-1, SIRT1, and NF-kappaB. Cisplatin 167-176 nuclear factor kappa B subunit 1 Homo sapiens 263-272 26300057-0 2015 Silencing of PKC-alpha, TRPC1 or NF-kappaB expression attenuates cisplatin-induced ICAM-1 expression and endothelial dysfunction. Cisplatin 65-74 nuclear factor kappa B subunit 1 Homo sapiens 33-42 26429874-5 2015 So we speculated URGCP/URG4 regulates cisplatin-induced apoptosis by activating NF-kappaB pathway. Cisplatin 38-47 nuclear factor kappa B subunit 1 Homo sapiens 80-89 26429874-7 2015 In summary, URGCP/URG4 promotes the resistance to cisplatin-induced apoptosis by activating NF-kappaB pathway, and is an unfavorable prognostic factor for bladder cancer. Cisplatin 50-59 nuclear factor kappa B subunit 1 Homo sapiens 92-101 26693062-9 2015 These results indicated that IKK/NF-kappaB plays a pivotal role in controlling acquired cisplatin resistance and that targeting the IKK/NF-kappaB signaling pathway may provide a possible therapeutic method to overcome the acquired resistance to cisplatin in HNSCC. Cisplatin 88-97 nuclear factor kappa B subunit 1 Homo sapiens 33-42 26693062-9 2015 These results indicated that IKK/NF-kappaB plays a pivotal role in controlling acquired cisplatin resistance and that targeting the IKK/NF-kappaB signaling pathway may provide a possible therapeutic method to overcome the acquired resistance to cisplatin in HNSCC. Cisplatin 88-97 nuclear factor kappa B subunit 1 Homo sapiens 136-145 26693062-7 2015 Furthermore, knockdown of NF-kappaB or overexpression of p65-S536 alanine (p65-S536A) mutant sensitizes resistant cells to cisplatin. Cisplatin 123-132 nuclear factor kappa B subunit 1 Homo sapiens 26-35 26693062-9 2015 These results indicated that IKK/NF-kappaB plays a pivotal role in controlling acquired cisplatin resistance and that targeting the IKK/NF-kappaB signaling pathway may provide a possible therapeutic method to overcome the acquired resistance to cisplatin in HNSCC. Cisplatin 245-254 nuclear factor kappa B subunit 1 Homo sapiens 33-42 26693062-9 2015 These results indicated that IKK/NF-kappaB plays a pivotal role in controlling acquired cisplatin resistance and that targeting the IKK/NF-kappaB signaling pathway may provide a possible therapeutic method to overcome the acquired resistance to cisplatin in HNSCC. Cisplatin 245-254 nuclear factor kappa B subunit 1 Homo sapiens 136-145 25799148-0 2015 Modulation of NF-kappaB/miR-21/PTEN pathway sensitizes non-small cell lung cancer to cisplatin. Cisplatin 85-94 nuclear factor kappa B subunit 1 Homo sapiens 14-23 26118633-0 2015 Saikosaponin-D reduces cisplatin-induced nephrotoxicity by repressing ROS-mediated activation of MAPK and NF-kappaB signalling pathways. Cisplatin 23-32 nuclear factor kappa B subunit 1 Homo sapiens 106-115 26118633-7 2015 More importantly, SSD effectively blocked the DDP-induced activation of NF-kappaB, P38, JNK, and MAPKs. Cisplatin 46-49 nuclear factor kappa B subunit 1 Homo sapiens 72-81 26617729-0 2015 Activation of unfolded protein response protects osteosarcoma cells from cisplatin-induced apoptosis through NF-kappaB pathway. Cisplatin 73-82 nuclear factor kappa B subunit 1 Homo sapiens 109-118 26617729-8 2015 Moreover, mechanistic investigation uncovered that cisplatin promoted the levels of nuclear NF-kappaB whereas 4-PBA administration suppressed the cisplatin-induced accumulation of nuclear NF-kappaB level in osteosarcoma cells. Cisplatin 51-60 nuclear factor kappa B subunit 1 Homo sapiens 92-101 26617729-8 2015 Moreover, mechanistic investigation uncovered that cisplatin promoted the levels of nuclear NF-kappaB whereas 4-PBA administration suppressed the cisplatin-induced accumulation of nuclear NF-kappaB level in osteosarcoma cells. Cisplatin 146-155 nuclear factor kappa B subunit 1 Homo sapiens 188-197 26617729-10 2015 Taken together, our data show that UPR protects osteosarcoma from cisplatin-mediated apoptosis through activation of NF-kappaB pathway. Cisplatin 66-75 nuclear factor kappa B subunit 1 Homo sapiens 117-126 26055133-1 2015 Nakai ex Kitam ethanol extract against cisplatin-induced apoptosis of human HaCaT keratinocytes: Involvement of NF-kappa B- and Bcl-2-controlled mitochondrial signaling. Cisplatin 39-48 nuclear factor kappa B subunit 1 Homo sapiens 112-122 25681684-5 2015 Using isogenic cellular matrices of cisplatin, paclitaxel and platinum-taxol resistant MyD88(negative) A2780 ovarian cancer cells expressing a NF-kappaB reporter sensor, we showed that enhanced NF-kappaB activity was required for cisplatin but not for paclitaxel resistance. Cisplatin 36-45 nuclear factor kappa B subunit 1 Homo sapiens 194-203 25681684-5 2015 Using isogenic cellular matrices of cisplatin, paclitaxel and platinum-taxol resistant MyD88(negative) A2780 ovarian cancer cells expressing a NF-kappaB reporter sensor, we showed that enhanced NF-kappaB activity was required for cisplatin but not for paclitaxel resistance. Cisplatin 230-239 nuclear factor kappa B subunit 1 Homo sapiens 194-203 25681684-6 2015 Immunofluorescence and gel mobility shift assay demonstrated enhanced nuclear localization of NF-kappaB and subsequent binding to NF-kappaB response element in cisplatin resistant cells. Cisplatin 160-169 nuclear factor kappa B subunit 1 Homo sapiens 94-103 25681684-6 2015 Immunofluorescence and gel mobility shift assay demonstrated enhanced nuclear localization of NF-kappaB and subsequent binding to NF-kappaB response element in cisplatin resistant cells. Cisplatin 160-169 nuclear factor kappa B subunit 1 Homo sapiens 130-139 25681684-9 2015 Intriguingly, silencing of MyD88 in cisplatin resistant and MyD88(positive) TOV21G and SKOV3 cells showed enhanced NF-kappaB activity after cisplatin but not after paclitaxel or platinum-taxol treatments. Cisplatin 36-45 nuclear factor kappa B subunit 1 Homo sapiens 115-124 25681684-9 2015 Intriguingly, silencing of MyD88 in cisplatin resistant and MyD88(positive) TOV21G and SKOV3 cells showed enhanced NF-kappaB activity after cisplatin but not after paclitaxel or platinum-taxol treatments. Cisplatin 140-149 nuclear factor kappa B subunit 1 Homo sapiens 115-124 25681684-10 2015 Our data thus suggest that NF-kappaB signaling is important for maintenance of cisplatin resistance but not for taxol or platinum-taxol resistance in absence of an active TLR-4/MyD88 receptor mediated cell survival pathway in epithelial ovarian carcinoma. Cisplatin 79-88 nuclear factor kappa B subunit 1 Homo sapiens 27-36 25799148-2 2015 Our present study was aimed to determine whether inhibition of the NF-kappaB/miR-21/PTEN pathway could increase the sensitivity of NSCLC to cisplatin. Cisplatin 140-149 nuclear factor kappa B subunit 1 Homo sapiens 67-76 25799148-7 2015 Finally, we measured the cell viability and apoptosis under cisplatin treatment when NF-kappaB was inhibited. Cisplatin 60-69 nuclear factor kappa B subunit 1 Homo sapiens 85-94 25799148-12 2015 Hence, inhibition of NF-kappaB by RNA silencing protects cells against cisplatin via decreasing miR-21 expression. Cisplatin 71-80 nuclear factor kappa B subunit 1 Homo sapiens 21-30 25799148-13 2015 CONCLUSION: Modulation of the NF-kappaB/miR-21/PTEN pathway in NSCLC showed that inhibition of this pathway may increase cisplatin sensitivity. Cisplatin 121-130 nuclear factor kappa B subunit 1 Homo sapiens 30-39 24988892-5 2014 Most importantly, lung cancer cells themselves upregulated IL-6 secretion by activating the p38/NF-kappaB pathway through treatment with cisplatin and camptothecin. Cisplatin 137-146 nuclear factor kappa B subunit 1 Homo sapiens 96-105 25499851-0 2015 MnSOD overexpression confers cisplatin resistance in lung adenocarcinoma via the NF-kappaB/Snail/Bcl-2 pathway. Cisplatin 29-38 nuclear factor kappa B subunit 1 Homo sapiens 81-90 25499851-3 2015 Therefore, we hypothesized that MnSOD-mediated NF-kappaB activation might confer cisplatin resistance in lung adenocarcinoma via the NF-kappaB/Bcl-2/Snail pathway. Cisplatin 81-90 nuclear factor kappa B subunit 1 Homo sapiens 47-56 25499851-3 2015 Therefore, we hypothesized that MnSOD-mediated NF-kappaB activation might confer cisplatin resistance in lung adenocarcinoma via the NF-kappaB/Bcl-2/Snail pathway. Cisplatin 81-90 nuclear factor kappa B subunit 1 Homo sapiens 133-142 25499851-6 2015 Mechanistically, an increase in Bcl-2 by MnSOD-mediated NF-kappaB activation confers greater cisplatin resistance than cIAP2, Bcl-xL, Mcl-1, and Snail. Cisplatin 93-102 nuclear factor kappa B subunit 1 Homo sapiens 56-65 25348361-0 2015 DNA-PKcs deficiency sensitizes the human hepatoma HepG2 cells to cisplatin and 5-fluorouracil through suppression of the PI3K/Akt/NF-kappaB pathway. Cisplatin 65-74 nuclear factor kappa B subunit 1 Homo sapiens 130-139 25348361-7 2015 Moreover, CDDP could inhibit the transcriptional activity of NF-kappaB through degradation of IkB-alpha, while 5-Fu alone seemed in some extent increases the NF-kappaB activity. Cisplatin 10-14 nuclear factor kappa B subunit 1 Homo sapiens 61-70 25348361-8 2015 The combined treatment with CDDP and 5-Fu resulted in significantly decrease of the transcriptional activity of NF-kappaB, which was further aggravated by DNA-PKcs siRNA treatment. Cisplatin 28-32 nuclear factor kappa B subunit 1 Homo sapiens 112-121 25348361-9 2015 In conclusion, DNA-PKcs suppression had complementary effects in combination with CDDP and 5-Fu treatment in HepG2 cells, which was associated with suppression of NF-kappaB signaling pathway cascade, activation of caspase-3 and p53, as well as down-regulation of Bcl-2 and GSH. Cisplatin 82-86 nuclear factor kappa B subunit 1 Homo sapiens 163-172 25331947-0 2014 p16 Protein and gigaxonin are associated with the ubiquitination of NFkappaB in cisplatin-induced senescence of cancer cells. Cisplatin 80-89 nuclear factor kappa B subunit 1 Homo sapiens 68-76 25331947-2 2014 Here we show that cisplatin treatment of head and neck cancer cells results in nuclear transport of p16 leading to a molecular modification of NFkappaB. Cisplatin 18-27 nuclear factor kappa B subunit 1 Homo sapiens 143-151 25331947-7 2014 Furthermore, we have observed increased NFkappaB ubiquitination with cisplatin treatment that is abolished in the absence of p16 and gigaxonin expression. Cisplatin 69-78 nuclear factor kappa B subunit 1 Homo sapiens 40-48 25025901-0 2014 Strategic targeting of the PI3K-NFkappaB axis in cisplatin-resistant NSCLC. Cisplatin 49-58 nuclear factor kappa B subunit 1 Homo sapiens 32-40 25025901-3 2014 In this study, targeted inhibition of three strategic points of the PI3K-NFkappaB axis was performed with the aim of exploiting vulnerabilities in cisplatin-resistant NSCLC cells. Cisplatin 147-156 nuclear factor kappa B subunit 1 Homo sapiens 73-81 25025901-5 2014 Expression of PI3K and NFkappaB pathway-related genes were compared between cisplatin-resistant cells and their matched parent cells using a gene expression array, qRT-PCR, DNA sequencing, western blot, and immunofluorescence. Cisplatin 76-85 nuclear factor kappa B subunit 1 Homo sapiens 23-31 24594834-7 2014 In addition, PDTC blocked cisplatin-induced activation of NF-kappaB, leading to enhanced apoptosis and increased chemosensitivity to cisplatin. Cisplatin 26-35 nuclear factor kappa B subunit 1 Homo sapiens 58-67 24594834-7 2014 In addition, PDTC blocked cisplatin-induced activation of NF-kappaB, leading to enhanced apoptosis and increased chemosensitivity to cisplatin. Cisplatin 133-142 nuclear factor kappa B subunit 1 Homo sapiens 58-67 25462204-8 2015 In addition, a combination of PREC and cisplatin-induced ovarian cancer cell apoptosis by downregulating the Akt and NFkappaB pathways. Cisplatin 39-48 nuclear factor kappa B subunit 1 Homo sapiens 117-125 26491668-5 2015 We found that the synergistic inhibitory effects of cetuximab and cisplatin on AP-1 and NF-kappaB activation, as well as on cell viability, were reversed by pretreatment with an ERK inhibitor. Cisplatin 66-75 nuclear factor kappa B subunit 1 Homo sapiens 88-97 26491668-6 2015 Results demonstrate that combined treatment with cetuximab and cisplatin exerts synergistic anticancer effects on colon cancer cells and also suggest that the ERK pathway plays a critical role in these effects via the suppression of the EGFR signaling pathway, along with the inhibition of COX-2, IL-8, and AP-1 and NF-kappaB. Cisplatin 63-72 nuclear factor kappa B subunit 1 Homo sapiens 316-325 24981574-8 2014 Mutation of the p53 response element from GGGCAGAGCCC to GGGCACC or mutation of the NFkappaB response element from GGAAAGTCC to GGAAAGGAA by site-directed mutagenesis abolished the stimulation of cisplatin on the BTG2 promoter activity in LNCaP or PC-3 cells, respectively. Cisplatin 196-205 nuclear factor kappa B subunit 1 Homo sapiens 84-92 25145705-10 2014 CONCLUSIONS: Upregulation of TBL1XR1 induces NPC cells resistance to cisplatin by activating the NF-kappaB pathway, and correlates with poor overall survival of NPC patients. Cisplatin 69-78 nuclear factor kappa B subunit 1 Homo sapiens 97-106 25145705-0 2014 Transducin beta-like 1 X-linked receptor 1 suppresses cisplatin sensitivity in nasopharyngeal carcinoma via activation of NF-kappaB pathway. Cisplatin 54-63 nuclear factor kappa B subunit 1 Homo sapiens 122-131 24960055-9 2014 Taken together, HBCD and PCBs at low concentrations could increase the resistance of HCC cells to cisplatin through modulation on NF-kappaB pathway activation and p53 function, which is associated with the activity of PI3K/Akt pathway. Cisplatin 98-107 nuclear factor kappa B subunit 1 Homo sapiens 130-139 25068924-10 2014 A combination treatment of tumor necrosis factor (TNF)-like weak inducer of apoptosis, TNF-related apoptosis-inducing ligand, docetaxel and cisplatin, with BV synergistically inhibited both A549 and NCI-H460 lung cancer cell growth with further down regulation of NF-kappaB activity. Cisplatin 140-149 nuclear factor kappa B subunit 1 Homo sapiens 264-273 24981574-9 2014 Our results indicated that cisplatin attenuates prostate cancer cell proliferation partly mediated by upregulation of BTG2 through the p53-dependent pathway or p53-independent NFkappaB pathway. Cisplatin 27-36 nuclear factor kappa B subunit 1 Homo sapiens 176-184 24581167-6 2014 CONCLUSION: Vinorelbine treatment led to increase of cisplatin sensitivity of A549/DDP cells and the mechanisms included the regulation of PTEN/AKT/NF-kappaB signal pathway to decreased drug resistance gene expression and increased pro-apoptosis gene expression. Cisplatin 53-62 nuclear factor kappa B subunit 1 Homo sapiens 148-157 24854552-13 2014 CONCLUSIONS: IKBKB inhibits cisplatin-induced apoptosis via the activation of NF-kappaB pathway. Cisplatin 28-37 nuclear factor kappa B subunit 1 Homo sapiens 78-87 24418212-3 2014 Although the kB site-NF-kappaB protein interaction was significantly perturbed by DNA adducts of cisplatin, transplatin adducts were markedly less effective both in cell-free media and in cellulo using a decoy strategy derivatized-approach. Cisplatin 97-106 nuclear factor kappa B subunit 1 Homo sapiens 21-30 24418212-4 2014 Moreover, NF-kappaB inhibitor JSH-23 [4-methyl-N1-(3-phenylpropyl)benzene-1,2-diamine] augmented cisplatin cytotoxicity in ovarian cancer cells and the data showed strong synergy with JSH-23 for cisplatin. Cisplatin 97-106 nuclear factor kappa B subunit 1 Homo sapiens 10-19 24418212-4 2014 Moreover, NF-kappaB inhibitor JSH-23 [4-methyl-N1-(3-phenylpropyl)benzene-1,2-diamine] augmented cisplatin cytotoxicity in ovarian cancer cells and the data showed strong synergy with JSH-23 for cisplatin. Cisplatin 195-204 nuclear factor kappa B subunit 1 Homo sapiens 10-19 24418212-6 2014 Because thousands of kappaB sites are present in the DNA, the mechanisms underlying the antitumor efficiency of cisplatin in some tumor cells may involve downstream processes after inhibition of the binding of NF-kappaB to kappaB site(s) by DNA adducts of cisplatin, including enhanced programmed cell death in response to drug treatment. Cisplatin 112-121 nuclear factor kappa B subunit 1 Homo sapiens 210-219 24418212-6 2014 Because thousands of kappaB sites are present in the DNA, the mechanisms underlying the antitumor efficiency of cisplatin in some tumor cells may involve downstream processes after inhibition of the binding of NF-kappaB to kappaB site(s) by DNA adducts of cisplatin, including enhanced programmed cell death in response to drug treatment. Cisplatin 256-265 nuclear factor kappa B subunit 1 Homo sapiens 210-219 24490130-0 2014 NFkappaB mediates cisplatin resistance through histone modifications in head and neck squamous cell carcinoma (HNSCC). Cisplatin 18-27 nuclear factor kappa B subunit 1 Homo sapiens 0-8 24300974-0 2014 Gambogic acid synergistically potentiates cisplatin-induced apoptosis in non-small-cell lung cancer through suppressing NF-kappaB and MAPK/HO-1 signalling. Cisplatin 42-51 nuclear factor kappa B subunit 1 Homo sapiens 120-129 24300974-8 2014 Importantly, it was found that, followed by CDDP treatment, GA could inhibit NF-kappaB and mitogen-activated protein kinase (MAPK)/heme oxygenase-1 (HO-1) signalling pathways, which have been validated to reduce ROS release and confer CDDP resistance. Cisplatin 44-48 nuclear factor kappa B subunit 1 Homo sapiens 77-86 24300974-9 2014 The roles of NF-kappaB and MAPK pathways were further confirmed by using specific inhibitors, which significantly increased ROS release and apoptosis induced by the sequential combination of CDDP and GA. Cisplatin 191-195 nuclear factor kappa B subunit 1 Homo sapiens 13-22 24300974-10 2014 Moreover, our results indicated that the combination of CDDP and GA exerted increased antitumour effects on A549 xenograft models through inhibiting NF-kappaB, HO-1, and subsequently inducing apoptosis. Cisplatin 56-60 nuclear factor kappa B subunit 1 Homo sapiens 149-158 24490130-8 2014 We found that pharmacological induction of histone acetylation using HDAC inhibitors prevented NFkappaB-induced cisplatin resistance. Cisplatin 112-121 nuclear factor kappa B subunit 1 Homo sapiens 95-103 24490130-9 2014 Furthermore, silencing NFkappaB in HNSCC induced acetylation of tumor histones, resulting in reduced chemoresistance and increased cytotoxicity following cisplatin treatment. Cisplatin 154-163 nuclear factor kappa B subunit 1 Homo sapiens 23-31 23381786-0 2013 Camptothecin and cisplatin upregulate ABCG2 and MRP2 expression by activating the ATM/NF-kappaB pathway in lung cancer cells. Cisplatin 17-26 nuclear factor kappa B subunit 1 Homo sapiens 86-95 23880825-9 2013 The cisplatin resistance was demonstrated to be caused by increased AKT and NFkappaB activity induced by C35-DeltaNp73. Cisplatin 4-13 nuclear factor kappa B subunit 1 Homo sapiens 76-84 23545383-4 2013 The present study focused on investigating important cell signaling molecules such as Akt and NF-kappaB during salinomycin-induced apoptosis in cisplatin resistant ovarian cancer cells (A2780cis). Cisplatin 144-153 nuclear factor kappa B subunit 1 Homo sapiens 94-103 23720710-6 2013 Here, we describe the role of NF-kappaB in cancer and in the development of resistance, particularly cisplatin. Cisplatin 101-110 nuclear factor kappa B subunit 1 Homo sapiens 30-39 23381786-2 2013 Our study showed that both camptothecin and cisplatin could not only induce ATM and NF-kappaB activation but also upregulate expression of the MDR-related genes ABCG2, MRP2 in NCI-H446 cells. Cisplatin 44-53 nuclear factor kappa B subunit 1 Homo sapiens 84-93 23381786-3 2013 Moreover, camptothecin and cisplatin-induced ABCG2 and MRP2 upregulation could be impaired by ATM and NF-kappaB inhibitors, indicating a relationship between ATM, NF-kappaB activation and MDR formation in lung cancer chemo-therapy. Cisplatin 27-36 nuclear factor kappa B subunit 1 Homo sapiens 102-111 23381786-3 2013 Moreover, camptothecin and cisplatin-induced ABCG2 and MRP2 upregulation could be impaired by ATM and NF-kappaB inhibitors, indicating a relationship between ATM, NF-kappaB activation and MDR formation in lung cancer chemo-therapy. Cisplatin 27-36 nuclear factor kappa B subunit 1 Homo sapiens 163-172 23103562-0 2013 TNF-alpha-mediated NF-kappaB survival signaling impairment by cisplatin enhances JNK activation allowing synergistic apoptosis of renal proximal tubular cells. Cisplatin 62-71 nuclear factor kappa B subunit 1 Homo sapiens 19-28 23886095-10 2013 CONCLUSIONS: TCS could enhance cisplatin-induced apoptosis in Hep-2 and AMC-HN-8, at least in part, by inhibiting the NF-kappaB signaling pathway and activating JNK/SAPK signaling pathway and thus strengthening the antitumor effects of cisplatin, which highlights the possibility of combined application of TCS and cisplatin in the treatment of laryngeal carcinoma. Cisplatin 31-40 nuclear factor kappa B subunit 1 Homo sapiens 118-127 23103562-8 2013 Furthermore, combined cisplatin/TNF-alpha treatment inhibited NF-kappaB nuclear translocation and NF-kappaB-mediated gene transcription leading to enhanced and prolonged JNK and c-Jun phosphorylation. Cisplatin 22-31 nuclear factor kappa B subunit 1 Homo sapiens 62-71 23103562-8 2013 Furthermore, combined cisplatin/TNF-alpha treatment inhibited NF-kappaB nuclear translocation and NF-kappaB-mediated gene transcription leading to enhanced and prolonged JNK and c-Jun phosphorylation. Cisplatin 22-31 nuclear factor kappa B subunit 1 Homo sapiens 98-107 23103562-10 2013 This led to an alteration in the transcription of the NF-kappaB-induced anti-apoptotic genes c-IAP2, Bcl-XL, Bruce and Bcl2 and pro-apoptotic genes Bfk and Xaf1 and consequently to sensitization of the IM-PTECs toward cisplatin/TNF-alpha-induced toxicity. Cisplatin 218-227 nuclear factor kappa B subunit 1 Homo sapiens 54-63 23103562-11 2013 In conclusion, our findings support a model whereby renal cells exposed to both cisplatin and TNF-alpha switch into a more pro-apoptotic and inflammatory program by altering their NF-kappaB/JNK/c-Jun balance. Cisplatin 80-89 nuclear factor kappa B subunit 1 Homo sapiens 180-189 23299493-0 2013 Fucoxanthin enhances cisplatin-induced cytotoxicity via NFkappaB-mediated pathway and downregulates DNA repair gene expression in human hepatoma HepG2 cells. Cisplatin 21-30 nuclear factor kappa B subunit 1 Homo sapiens 56-64 23299493-5 2013 Mechanistically, we showed that fucoxanthin attenuated cisplatin-induced NFkappaB expression and enhanced the NFkappaB-regulated Bax/Bcl-2 mRNA ratio. Cisplatin 55-64 nuclear factor kappa B subunit 1 Homo sapiens 73-81 22330808-0 2012 SIRT1 overexpression decreases cisplatin-induced acetylation of NF-kappaB p65 subunit and cytotoxicity in renal proximal tubule cells. Cisplatin 31-40 nuclear factor kappa B subunit 1 Homo sapiens 64-73 22562377-12 2012 Our results suggest that the high cisplatin resistance of KCP-4 cells compared with KB-3-1 cells results from multiple mechanisms other than increased cisplatin efflux, including the activation of NF-kappaB. Cisplatin 34-43 nuclear factor kappa B subunit 1 Homo sapiens 197-206 23886095-8 2013 Western blot showed the expression of p-JNK/SAPK significantly increased in the cells treated with 5 microg/ml TCS for 48 hours, while the expression of NF-kappaB and phospho-I-kappaB increased in the cells treated with 3 microg/ml cisplatin. Cisplatin 232-241 nuclear factor kappa B subunit 1 Homo sapiens 153-162 23886095-9 2013 However in the cells treated with 5 microg/ml TCS combined with 3 microg/ml cisplatin, the expression of p-JNK stayed at a high level and the expressions of NF-kappaB and phospho-I-kappaB decreased dramatically compared to the cells treated with 3 microg/ml cisplatin alone. Cisplatin 76-85 nuclear factor kappa B subunit 1 Homo sapiens 157-166 23600205-0 2013 [Effects of NF-kappaB inhibitor on cisplatin-induced apoptosis in cervical cancer]. Cisplatin 35-44 nuclear factor kappa B subunit 1 Homo sapiens 12-21 23600205-1 2013 OBJECTIVE: To observe whether cisplatin-induced apoptosis were increased when SiHa cells were preincubated with nuclear factor-kappa B (NF-kappaB) inhibitors [aspirin, sulindac, curcumin or pyrrolidine dithiocarbamate (PDTC)]. Cisplatin 30-39 nuclear factor kappa B subunit 1 Homo sapiens 112-134 23600205-1 2013 OBJECTIVE: To observe whether cisplatin-induced apoptosis were increased when SiHa cells were preincubated with nuclear factor-kappa B (NF-kappaB) inhibitors [aspirin, sulindac, curcumin or pyrrolidine dithiocarbamate (PDTC)]. Cisplatin 30-39 nuclear factor kappa B subunit 1 Homo sapiens 136-145 23600205-7 2013 MTT assay demonstrated that a preincubation with NF-kappaB inhibitor could signifianctly increase cisplatin-induced chemosensitivity (P < 0.05). Cisplatin 98-107 nuclear factor kappa B subunit 1 Homo sapiens 49-58 23600205-10 2013 CONCLUSION: Aspirin, sulindac, curcumin and PDTC could all inhibit cisplatin induced NF-kappaB activiation, which could increase cispaltin-induced chemosensativity by augments of apoptosis. Cisplatin 67-76 nuclear factor kappa B subunit 1 Homo sapiens 85-94 22753722-6 2012 These results suggest that down-regulation of Notch-1, via inhibition of NF-kappaB signaling pathways by delta-tocotrienol and cisplatin, in combination, could provide a potential novel approach for tumor arrest in NSCLC, while lowering the effective dose of cisplatin. Cisplatin 127-136 nuclear factor kappa B subunit 1 Homo sapiens 73-82 22562377-0 2012 Involvement of NF-kappaB activation in the cisplatin resistance of human epidermoid carcinoma KCP-4 cells. Cisplatin 43-52 nuclear factor kappa B subunit 1 Homo sapiens 15-24 22562377-6 2012 The aim of this study was to investigate whether the activation of nuclear factor-kappa B (NF-kappaB) contributes to the cisplatin resistance of KCP-4 cells. Cisplatin 121-130 nuclear factor kappa B subunit 1 Homo sapiens 67-89 22562377-6 2012 The aim of this study was to investigate whether the activation of nuclear factor-kappa B (NF-kappaB) contributes to the cisplatin resistance of KCP-4 cells. Cisplatin 121-130 nuclear factor kappa B subunit 1 Homo sapiens 91-100 22417828-4 2012 Inhibition of NF-kappaB activity by chemical inhibitor or overexpression of Ikappa-Balpha in Cdc25A-elevated cancer cells resistant to cisplatin improved their sensitivity to cisplatin-induced apoptosis. Cisplatin 135-144 nuclear factor kappa B subunit 1 Homo sapiens 14-23 22417828-4 2012 Inhibition of NF-kappaB activity by chemical inhibitor or overexpression of Ikappa-Balpha in Cdc25A-elevated cancer cells resistant to cisplatin improved their sensitivity to cisplatin-induced apoptosis. Cisplatin 175-184 nuclear factor kappa B subunit 1 Homo sapiens 14-23 22330808-6 2012 While protein expression of SIRT1 was decreased by cisplatin treatment compared with control buffer treatment, acetylation of NF-kappaB p65 subunit was significantly increased after treatment with cisplatin. Cisplatin 197-206 nuclear factor kappa B subunit 1 Homo sapiens 126-135 22330808-7 2012 Overexpression of SIRT1 ameliorated the increased acetylation of p65 of NF-kappaB during cisplatin treatment and cisplatin-induced cytotoxicity. Cisplatin 89-98 nuclear factor kappa B subunit 1 Homo sapiens 72-81 22330808-8 2012 Further, treatment of cisplatin-treated HK2 cells with resveratrol, a SIRT1 activator, also decreased acetylation of NF-kappaB p65 subunit and cisplatin-induced increase of the cell viability in HK2 cells. Cisplatin 22-31 nuclear factor kappa B subunit 1 Homo sapiens 117-126 22330808-9 2012 Our findings suggests that the regulation of acetylation of p65 of NF-kappaB through SIRT1 can be a possible target to attenuate cisplatin-induced renal cell damage. Cisplatin 129-138 nuclear factor kappa B subunit 1 Homo sapiens 67-76 23056046-8 2012 The results in the present study suggest that genistein could enhance the activity of cisplatin via inhibition of NF-kappaB and Akt/mTOR pathways. Cisplatin 86-95 nuclear factor kappa B subunit 1 Homo sapiens 114-123 21614498-4 2012 RESULTS: Our results showed that expression of AQP5, NF-kappaB in cytoplasm and karyon and IkappaBalpha in cytoplasm protein in CAOV3 cells can be induced to decrease by cisplatin with concentration-dependent manner, and there is a positive correlation between AQP5 protein and cell growth rate (r = 0.607, P < 0.05). Cisplatin 170-179 nuclear factor kappa B subunit 1 Homo sapiens 53-62 21614498-5 2012 When cells were incubated with 10 mug/ml cisplatin, AQP5, NF-kappaB p65, and IkappaBalpha increased rapidly at 6-12 h, but decreased at 24 h, remain on low level until to 72 h. Expression of AQP5 could be induced to decrease by PDTC, and a positive correlation between AQP5 protein expression and NF-kappaB p65 and IkappaBalpha (r = 0.894, 0.857; P < 0.05). Cisplatin 41-50 nuclear factor kappa B subunit 1 Homo sapiens 58-67 22417828-2 2012 Here we report that Cdc25A inhibits cisplatin-induced apoptotic cell death by stimulating nuclear factor-kappa B (NF-kappaB) activity. Cisplatin 36-45 nuclear factor kappa B subunit 1 Homo sapiens 90-112 22417828-2 2012 Here we report that Cdc25A inhibits cisplatin-induced apoptotic cell death by stimulating nuclear factor-kappa B (NF-kappaB) activity. Cisplatin 36-45 nuclear factor kappa B subunit 1 Homo sapiens 114-123 23251525-0 2012 Microarray-assisted pathway analysis identifies MT1X & NFkappaB as mediators of TCRP1-associated resistance to cisplatin in oral squamous cell carcinoma. Cisplatin 115-124 nuclear factor kappa B subunit 1 Homo sapiens 59-67 21945668-0 2011 Latent membrane protein 1 of Epstein-Barr virus sensitizes cancer cells to cisplatin by enhancing NF-kappaB p50 homodimer formation and downregulating NAPA expression. Cisplatin 75-84 nuclear factor kappa B subunit 1 Homo sapiens 98-107 21945668-0 2011 Latent membrane protein 1 of Epstein-Barr virus sensitizes cancer cells to cisplatin by enhancing NF-kappaB p50 homodimer formation and downregulating NAPA expression. Cisplatin 75-84 nuclear factor kappa B subunit 1 Homo sapiens 108-111 21945668-10 2011 These findings suggest that the viral protein LMP1 may sensitize cancer cells to cisplatin chemotherapy by downregulating NAPA and by enhancing the formation of p50 homodimers which in turn inhibit the expression of NF-kappaB regulated anti-apoptotic genes. Cisplatin 81-90 nuclear factor kappa B subunit 1 Homo sapiens 161-164 21945668-10 2011 These findings suggest that the viral protein LMP1 may sensitize cancer cells to cisplatin chemotherapy by downregulating NAPA and by enhancing the formation of p50 homodimers which in turn inhibit the expression of NF-kappaB regulated anti-apoptotic genes. Cisplatin 81-90 nuclear factor kappa B subunit 1 Homo sapiens 216-225 21088498-4 2010 We show that DeltaNp63alpha interacts with NF-kappaBeta in presence of cisplatin. Cisplatin 71-80 nuclear factor kappa B subunit 1 Homo sapiens 43-55 22074157-0 2011 Pentoxifylline sensitizes human cervical tumor cells to cisplatin-induced apoptosis by suppressing NF-kappa B and decreased cell senescence. Cisplatin 56-65 nuclear factor kappa B subunit 1 Homo sapiens 99-109 21570766-0 2011 RasGAP-derived peptide 38GAP potentiates the cytotoxicity of cisplatin through inhibitions of Akt, ERK and NF-kappaB in colon carcinoma HCT116 cells. Cisplatin 61-70 nuclear factor kappa B subunit 1 Homo sapiens 107-116 21570766-4 2011 This synergistic effect was associated with abrogation of CDDP-induced G2/M arrest by down-regulations of phospho-Cdc2 and p21, and inhibitions of phospho-AKT, phospho-ERK and NF-kappaB. Cisplatin 58-62 nuclear factor kappa B subunit 1 Homo sapiens 176-185 21617851-4 2011 However, the intensity of the induced AP-1 and NF-kappaB was diminished after cisplatin treatment, but not after TPA. Cisplatin 78-87 nuclear factor kappa B subunit 1 Homo sapiens 47-56 21040711-8 2011 Also, NFkappaB was found overstimulated in cisplatin-resistant C6 cells, and treatment of GBMs with NFkappaB inhibitors overcame cisplatin resistance besides potentiating the effects of the chemotherapeutics, cisplatin and doxorubicin. Cisplatin 43-52 nuclear factor kappa B subunit 1 Homo sapiens 6-14 21040711-8 2011 Also, NFkappaB was found overstimulated in cisplatin-resistant C6 cells, and treatment of GBMs with NFkappaB inhibitors overcame cisplatin resistance besides potentiating the effects of the chemotherapeutics, cisplatin and doxorubicin. Cisplatin 43-52 nuclear factor kappa B subunit 1 Homo sapiens 100-108 21040711-8 2011 Also, NFkappaB was found overstimulated in cisplatin-resistant C6 cells, and treatment of GBMs with NFkappaB inhibitors overcame cisplatin resistance besides potentiating the effects of the chemotherapeutics, cisplatin and doxorubicin. Cisplatin 129-138 nuclear factor kappa B subunit 1 Homo sapiens 100-108 21040711-8 2011 Also, NFkappaB was found overstimulated in cisplatin-resistant C6 cells, and treatment of GBMs with NFkappaB inhibitors overcame cisplatin resistance besides potentiating the effects of the chemotherapeutics, cisplatin and doxorubicin. Cisplatin 129-138 nuclear factor kappa B subunit 1 Homo sapiens 100-108 20207071-3 2010 In the present study, we investigate the activation of the NF-kappaB and Akt pathways by two frontline anticancer drugs cisplatin and etopside in a variety of cancer cell lines. Cisplatin 120-129 nuclear factor kappa B subunit 1 Homo sapiens 59-68 19553005-8 2009 Treatment with the PI3K inhibitor LY294002 or the NF-kappaB inhibitor BAY11-7082 enhanced cisplatin antitumor activity in parental H1299 cells but only weakly affected responses of H727 and H460 cells. Cisplatin 90-99 nuclear factor kappa B subunit 1 Homo sapiens 50-59 20207071-5 2010 The results show that cisplatin and etopside activate both NF-kappaB and Akt in cancer cells. Cisplatin 22-31 nuclear factor kappa B subunit 1 Homo sapiens 59-68 20594324-14 2010 TQ down regulated NF-kappaB expression which may explain its various cellular activities and this activity may prove useful in overcoming CDDP resistance from over expression of NF-kappaB. Cisplatin 138-142 nuclear factor kappa B subunit 1 Homo sapiens 18-27 20594324-14 2010 TQ down regulated NF-kappaB expression which may explain its various cellular activities and this activity may prove useful in overcoming CDDP resistance from over expression of NF-kappaB. Cisplatin 138-142 nuclear factor kappa B subunit 1 Homo sapiens 178-187 20372863-7 2010 Cisplatin treatment induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK expression, and suppressed Bcl-2 and Bcl-xl expression, whereas cells transfected with pcDNA3.1-ARL6IP1 showed lower levels of cisplatin-induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK up-regulation and higher levels of cisplatin-suppressed Bcl-2 and Bcl-xl down-regulation. Cisplatin 0-9 nuclear factor kappa B subunit 1 Homo sapiens 53-62 20372863-7 2010 Cisplatin treatment induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK expression, and suppressed Bcl-2 and Bcl-xl expression, whereas cells transfected with pcDNA3.1-ARL6IP1 showed lower levels of cisplatin-induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK up-regulation and higher levels of cisplatin-suppressed Bcl-2 and Bcl-xl down-regulation. Cisplatin 0-9 nuclear factor kappa B subunit 1 Homo sapiens 242-251 20372863-8 2010 These novel findings collectively suggest that ARL6IP1 may play a key role in cisplatin-induced apoptosis in CaSki cervical cancer cells by regulating the expression of apoptosis-associated proteins such as caspase-3, -9, p53, NF-kappaB, MAPK, Bcl-2, Bcl-xl, and Bax. Cisplatin 78-87 nuclear factor kappa B subunit 1 Homo sapiens 227-236 19908232-3 2010 Here, for the first time, we investigated the effects and mechanisms of NF-kappaB inhibition by ursolic acid on chemotherapy treatment (Taxol or cisplatin) of cancer. Cisplatin 145-154 nuclear factor kappa B subunit 1 Homo sapiens 72-81 20056115-6 2010 The combination of Rg3 (50 microM) with cisplatin (10 microM) and doxorubicin (2 microM) was also more effective in the inhibition of prostate cancer cell growth and NF-kappaB activity than those by the treatment of Rg3 or chemotherapeutics alone. Cisplatin 40-49 nuclear factor kappa B subunit 1 Homo sapiens 166-175 19856104-0 2010 Inhibition of nuclear factor kappa B transcription activity drives a synergistic effect of pyrrolidine dithiocarbamate and cisplatin for treatment of renal cell carcinoma. Cisplatin 123-132 nuclear factor kappa B subunit 1 Homo sapiens 14-36 19375813-3 2010 We found that treatment with cisplatin further augmented HO-1 expression, which was associated with activation of the epidermal growth factor receptor (EGFR) mediated signaling pathway and subsequent nuclear translocation of NF-kappaB. Cisplatin 29-38 nuclear factor kappa B subunit 1 Homo sapiens 225-234 19375813-7 2010 Collectively, the results indicate that resistance to cisplatin in A549 cells is associated with HO-1 through EGFR mediated signaling pathway including activation of the PI3k/Akt and NF-kappaB systems. Cisplatin 54-63 nuclear factor kappa B subunit 1 Homo sapiens 183-192 19553005-12 2009 Altogether, these results showed that either an activated PI3K/Akt/NF-kappaB pathway and/or high MKP1 was linked to reduced sensitivity to cisplatin in NSCLC cells. Cisplatin 139-148 nuclear factor kappa B subunit 1 Homo sapiens 67-76 19553005-13 2009 Inhibition of NF-kappaB or PI3K potently enhanced cisplatin cytotoxicity in cells with endogenous or genetically induced low MKP1 levels. Cisplatin 50-59 nuclear factor kappa B subunit 1 Homo sapiens 14-23 19553005-14 2009 These findings support the potential improvement in cisplatin responses by co-targeting NF-kappaB or Akt and MKP1. Cisplatin 52-61 nuclear factor kappa B subunit 1 Homo sapiens 88-97 19834284-6 2009 Similar combination effects of obovatol with other chemotherapeutic agents (paclitaxel, cisplatin, and doxorubicin) on the inhibition of cell growth and NF-kappaB activity were also found. Cisplatin 88-97 nuclear factor kappa B subunit 1 Homo sapiens 153-162 19723887-6 2009 Exposure of ESCC cells to two NF-kappaB inhibitors, Bay11-7082 and sulfasalazine, not only reduced cancer cell proliferation, but also induced apoptosis and enhanced sensitivity to chemotherapeutic drugs, 5-fluorouracil, and cisplatin. Cisplatin 225-234 nuclear factor kappa B subunit 1 Homo sapiens 30-39 19553005-0 2009 MKP1 repression is required for the chemosensitizing effects of NF-kappaB and PI3K inhibitors to cisplatin in non-small cell lung cancer. Cisplatin 97-106 nuclear factor kappa B subunit 1 Homo sapiens 64-73 19639202-5 2009 Low-dose cisplatin up-regulated hTERT and NF-kappaB p65 expression and increased telomerase and NF-kappaB activity. Cisplatin 9-18 nuclear factor kappa B subunit 1 Homo sapiens 42-51 19639202-5 2009 Low-dose cisplatin up-regulated hTERT and NF-kappaB p65 expression and increased telomerase and NF-kappaB activity. Cisplatin 9-18 nuclear factor kappa B subunit 1 Homo sapiens 96-105 19639202-6 2009 Inhibition of NF-kappaB attenuated the hTERT expression and telomerase activity exposed to cisplatin, suggesting that NF-kappaB is responsible for the cisplatin-induced activation of the hTERT. Cisplatin 91-100 nuclear factor kappa B subunit 1 Homo sapiens 14-23 19639202-6 2009 Inhibition of NF-kappaB attenuated the hTERT expression and telomerase activity exposed to cisplatin, suggesting that NF-kappaB is responsible for the cisplatin-induced activation of the hTERT. Cisplatin 91-100 nuclear factor kappa B subunit 1 Homo sapiens 118-127 19639202-6 2009 Inhibition of NF-kappaB attenuated the hTERT expression and telomerase activity exposed to cisplatin, suggesting that NF-kappaB is responsible for the cisplatin-induced activation of the hTERT. Cisplatin 151-160 nuclear factor kappa B subunit 1 Homo sapiens 14-23 19639202-6 2009 Inhibition of NF-kappaB attenuated the hTERT expression and telomerase activity exposed to cisplatin, suggesting that NF-kappaB is responsible for the cisplatin-induced activation of the hTERT. Cisplatin 151-160 nuclear factor kappa B subunit 1 Homo sapiens 118-127 19639202-9 2009 Taken together, these results suggested that up-regulation of hTERT expression by low-dose cisplatin is NF-kappaB-dependent and contributes to chemotherapy resistance in human hepatocellular cancer cells. Cisplatin 91-100 nuclear factor kappa B subunit 1 Homo sapiens 104-113 18942709-11 2009 This decreasing IC50 was correlated with the down-regulation of cisplatin-induced NF-kappaB activity in cyclin D1 knockdown cells, and was independent of CDK4 function. Cisplatin 64-73 nuclear factor kappa B subunit 1 Homo sapiens 82-91 19317621-7 2009 The results of our immunofluorescence staining indicated that a functional NER pathway was required for cisplatin-induced translocation of NF-kappaB p65 from cytoplasm into nucleus, indicative of NF-kappaB activation. Cisplatin 104-113 nuclear factor kappa B subunit 1 Homo sapiens 139-148 19317621-7 2009 The results of our immunofluorescence staining indicated that a functional NER pathway was required for cisplatin-induced translocation of NF-kappaB p65 from cytoplasm into nucleus, indicative of NF-kappaB activation. Cisplatin 104-113 nuclear factor kappa B subunit 1 Homo sapiens 196-205 19317621-8 2009 Given the important function of NF-kappaB in regulating transcription of the bcl-x(l) gene and the Bcl-x(L) protein in preventing apoptosis, these results suggest that NER may protect cells against cisplatin-induced apoptosis by activating NF-kappaB, which further induces transcription of the bcl-x(l) gene, resulting in an accumulation of Bcl-x(L) protein and activation of the cell survival pathway that leads to increased cell survival under cisplatin treatment. Cisplatin 198-207 nuclear factor kappa B subunit 1 Homo sapiens 32-41 19317621-8 2009 Given the important function of NF-kappaB in regulating transcription of the bcl-x(l) gene and the Bcl-x(L) protein in preventing apoptosis, these results suggest that NER may protect cells against cisplatin-induced apoptosis by activating NF-kappaB, which further induces transcription of the bcl-x(l) gene, resulting in an accumulation of Bcl-x(L) protein and activation of the cell survival pathway that leads to increased cell survival under cisplatin treatment. Cisplatin 198-207 nuclear factor kappa B subunit 1 Homo sapiens 240-249 18667446-7 2008 This implicates activation of NF-kappaB as the main cisplatin resistance mechanism downstream of TG2. Cisplatin 52-61 nuclear factor kappa B subunit 1 Homo sapiens 30-39 18607991-0 2008 Proapoptotic effects of NF-kappaB on cisplatin-induced cell death in auditory cell line. Cisplatin 37-46 nuclear factor kappa B subunit 1 Homo sapiens 24-33 18607991-1 2008 CONCLUSIONS: The findings suggest that nuclear factor (NF)-kappaB is activated by cisplatin and plays a proapoptotic role during cell death in the auditory cell line HEI-OC1. Cisplatin 82-91 nuclear factor kappa B subunit 1 Homo sapiens 39-65 18607991-4 2008 This study examined the role of NF-kappaB in the apoptotic pathway induced by cisplatin in the auditory cell line, HEI-OC1. Cisplatin 78-87 nuclear factor kappa B subunit 1 Homo sapiens 32-41 18607991-8 2008 After cisplatin treatment, NF-kappaB (p65) was activated to translocate from the cytoplasm into the nucleus. Cisplatin 6-15 nuclear factor kappa B subunit 1 Homo sapiens 27-36 18607991-9 2008 Co-treatment with NF-kappaB inhibitors reduced the cisplatin-induced apoptosis of HEI-OC1 cells. Cisplatin 51-60 nuclear factor kappa B subunit 1 Homo sapiens 18-27 18667446-9 2008 Our data show that TG2 prevents apoptosis induced by cisplatin by activating the NF-kappaB survival pathway in ovarian cancer cells. Cisplatin 53-62 nuclear factor kappa B subunit 1 Homo sapiens 81-90 18584244-2 2008 We report here that flunarizine markedly attenuates cisplatin-induced pro-inflammatory cytokine secretion and their messenger RNA transcription as well as cisplatin cytotoxicity through the activation of Nrf2/HO-1 and downregulation of NF-kappaB. Cisplatin 52-61 nuclear factor kappa B subunit 1 Homo sapiens 236-245 18563317-1 2008 Whether inhibiting the activity of nuclear factor (NF)-kappaB potentiates cisplatin-induced apoptosis in non-small cell lung cell line A549 cells was investigated. Cisplatin 74-83 nuclear factor kappa B subunit 1 Homo sapiens 35-61 18584244-5 2008 Flunarizine also attenuated cisplatin-mediated MAPK activation and pharmacological inhibition of MAPKs, especially MEK1/ERK, blocked cisplatin-induced NF-kappaB activation in HEI-OC1 cells. Cisplatin 28-37 nuclear factor kappa B subunit 1 Homo sapiens 151-160 18584244-5 2008 Flunarizine also attenuated cisplatin-mediated MAPK activation and pharmacological inhibition of MAPKs, especially MEK1/ERK, blocked cisplatin-induced NF-kappaB activation in HEI-OC1 cells. Cisplatin 133-142 nuclear factor kappa B subunit 1 Homo sapiens 151-160 18584244-8 2008 These results indicate that flunarizine induces a protective effect against cisplatin ototoxicity through the downregulation of NF-kappaB by Nrf2/HO-1 activation and the resulting inhibition of pro-inflammatory cytokine production in vitro and in vivo. Cisplatin 76-85 nuclear factor kappa B subunit 1 Homo sapiens 128-137