PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23665025-8 2013 We found that the combination of cisplatin and STAT3 siRNA resulted in the collapse of the mitochondrial membrane potential, attenuated the expression of Bcl-xL and Bcl-2, and increased the release of cytochrome C and expression of Bax. Cisplatin 33-42 BCL2 like 1 Homo sapiens 154-160 21252285-6 2011 Treatment with cisplatin/TRAIL also inhibited the expression of EGFR, p63, survivin, Bcl-2, and Bcl-xL in TNBC cells. Cisplatin 15-24 BCL2 like 1 Homo sapiens 96-102 22445428-3 2012 Here we show that cisplatin induced several platelet apoptotic events including up-regulation of Bax and Bak, down-regulation of Bcl-2 and Bcl-X(L), mitochondrial translocation of Bax, mitochondrial inner transmembrane potential depolarization, caspase-3 activation and phosphatidylserine (PS) exposure. Cisplatin 18-27 BCL2 like 1 Homo sapiens 139-147 22267549-10 2012 The involvement of Bcl-XL inhibition in sensitization was corroborated by the use of the pan-Bcl-2 inhibitor 2MAM-3 whereby the treated cells were sensitive to both CDDP- and TRAIL-induced apoptosis. Cisplatin 165-169 BCL2 like 1 Homo sapiens 19-25 21052098-4 2011 We demonstrated that Ad-ING4 plus CDDP induced synergistic growth inhibition, enhanced apoptosis, and had an additive effect on upregulation of Fas, Bax, Bak, cleaved Bid, cleaved caspase-8, caspase-9, caspase-3 and cleaved PARP, and on downregulation of Bcl-2 and Bcl-X(L) in SMMC-7721 hepatocarcinoma cells. Cisplatin 34-38 BCL2 like 1 Homo sapiens 265-273 23188704-5 2013 From among a panel of apoptosis-related factors (p53, Bcl-2, Bcl-XL, BAX, and survivin), the expression of Livin was upregulated after cisplatin treatment in a dose-dependent manner. Cisplatin 135-144 BCL2 like 1 Homo sapiens 61-67 22983390-11 2012 Furthermore, apoptotic proteins (PARP and caspase-3) and the anti-apoptotic protein Bcl-xL were modulated by the expression level of migfilin in combination with cisplatin. Cisplatin 162-171 BCL2 like 1 Homo sapiens 84-90 22431999-9 2012 In vitro studies demonstrated that MVs up-regulated in cisplatin-treated human tubular epithelial cells anti-apoptotic genes, such as Bcl-xL, Bcl2 and BIRC8 and down-regulated genes that have a central role in the execution-phase of cell apoptosis such as Casp1, Casp8 and LTA. Cisplatin 55-64 BCL2 like 1 Homo sapiens 134-140 21863213-0 2011 The p53 upregulated modulator of apoptosis (PUMA) chemosensitizes intrinsically resistant ovarian cancer cells to cisplatin by lowering the threshold set by Bcl-x(L) and Mcl-1. Cisplatin 114-123 BCL2 like 1 Homo sapiens 157-165 21863213-8 2011 Furthermore, PUMA chemosensitized intrinsically resistant SKOV3 cells to cisplatin through downregulation of B-cell lymphoma-extra large (Bcl-x(L)) and myeloid cell leukemia sequence 1 (Mcl-1). Cisplatin 73-82 BCL2 like 1 Homo sapiens 138-146 21863213-10 2011 To our knowledge, these data suggest a new mechanism by which overexpression of PUMA enhances sensitivity of SKOV3 cells to cisplatin by lowering the threshold set simultaneously by Bcl-x(L) and Mcl-1. Cisplatin 124-133 BCL2 like 1 Homo sapiens 182-190 20477830-8 2010 Knockdown of BCL2L1 abrogated the induced cisplatin-resistant phenotype. Cisplatin 42-51 BCL2 like 1 Homo sapiens 13-19 20142415-4 2010 Using RNA interference, we showed that Bcl-x(L) depletion sensitized two highly chemoresistant mesothelioma cell lines to cisplatin and that under this treatment, one cell line, MSTO-211H, displayed an apoptotic type of cell death, whereas the other, NCI-H28, evidenced mainly necrotic-type cell death. Cisplatin 122-131 BCL2 like 1 Homo sapiens 39-44 20619636-3 2010 In this study, we demonstrated that enforced expression of Aven blocks UV-irradiation-, SN-38- or cisplatin-induced apoptosis upstream of mitochondria by stabilising Bcl-xL protein levels in breast cancer cells. Cisplatin 98-107 BCL2 like 1 Homo sapiens 166-172 22545969-7 2010 beta-Elemene augmented the cisplatin-induced activation of caspase-3/7/10 and caspase-9, cleavage of caspase-3 and -9, suppression of Bcl-2 and Bcl-X(L) expression, and release of cytochrome c from mitochondria in these cells. Cisplatin 27-36 BCL2 like 1 Homo sapiens 144-152 20142415-5 2010 Otherwise, the inhibition of Mcl-1 by cisplatin may contribute to this induction of cell death observed after Bcl-x(L) downregulation. Cisplatin 38-47 BCL2 like 1 Homo sapiens 110-118 19887550-1 2009 Chemoresistance of ovarian carcinoma has been associated previously to the absence of Bcl-x(L) expression downregulation in response to cisplatin. Cisplatin 136-145 BCL2 like 1 Homo sapiens 86-94 20400521-6 2010 RESULTS: BLID was found to interact with Bcl-X(L), and the binding was enhanced in cancer cells exposed to doxorubicin or cisplatin. Cisplatin 122-131 BCL2 like 1 Homo sapiens 41-49 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 BCL2 like 1 Homo sapiens 109-115 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 BCL2 like 1 Homo sapiens 327-333 20451370-10 2010 Transcriptomic analyses by microarray show that VPA modulates transcription of genes (Na(+)/K(+) ATPase, Bcl-xL) involved in chemoresistance to cisplatin and etoposide. Cisplatin 144-153 BCL2 like 1 Homo sapiens 105-111 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 BCL2 like 1 Homo sapiens 251-257 19634140-2 2010 Cisplatin exposure of sensitive cells has been previously associated with a down-regulation of Bcl-X(L) expression and apoptosis, whereas recurrence was systematically observed when Bcl-X(L) expression was maintained. Cisplatin 0-9 BCL2 like 1 Homo sapiens 95-103 19634140-4 2010 We showed that a Bcl-X(L)targeted RNA interference strategy efficiently sensitized chemoresistant ovarian carcinoma cells to cisplatin, but some of them were still able to re-proliferate. Cisplatin 125-134 BCL2 like 1 Homo sapiens 17-25 19634140-8 2010 Moreover, we demonstrated that in presence of a low concentration of cisplatin, the concomitant down-regulation of Bcl-X(L) and MCL-1 allowed a complete annihilation of tumour cells population thus avoiding subsequent recurrence in vitro in cell lines highly refractory to any type of conventional chemotherapy. Cisplatin 69-78 BCL2 like 1 Homo sapiens 115-123 19934315-11 2009 Simultaneous downregulation of Bcl-x(L) was an additional requirement for cisplatin hypersensitivity, as p53-dependent cell death could be antagonized by exogenous Bcl-x(L). Cisplatin 74-83 BCL2 like 1 Homo sapiens 31-39 19934315-11 2009 Simultaneous downregulation of Bcl-x(L) was an additional requirement for cisplatin hypersensitivity, as p53-dependent cell death could be antagonized by exogenous Bcl-x(L). Cisplatin 74-83 BCL2 like 1 Homo sapiens 164-172 19578044-7 2009 Furthermore, p53 promotes cisplatin-induced apoptosis by directly binding and counteracting Bcl-x(L) antiapoptotic function. Cisplatin 26-35 BCL2 like 1 Homo sapiens 92-100 18585380-3 2008 Interestingly in one cisplatin resistant cell line which expresses BCL2/BCLxL, treatment with mTOR inhibitor (CCI-779) results in decreased levels of these anti-apoptotic proteins and may contribute to increasing apoptosis. Cisplatin 21-30 BCL2 like 1 Homo sapiens 72-77 19317621-0 2009 The role of Bcl-x(L) protein in nucleotide excision repair-facilitated cell protection against cisplatin-induced apoptosis. Cisplatin 95-104 BCL2 like 1 Homo sapiens 12-20 19317621-4 2009 We studied the role of the antiapoptotic Bcl-x(L) protein in nucleotide excision repair (NER)-facilitated cell protection against cisplatin-induced apoptosis. Cisplatin 130-139 BCL2 like 1 Homo sapiens 41-49 19317621-6 2009 The results obtained from our Western blots revealed that the cisplatin treatment led to an increase in the level of Bcl-x(L) protein in NF cells, but a decrease in the level of Bcl-x(L) protein in both XPA and XPG cells. Cisplatin 62-71 BCL2 like 1 Homo sapiens 117-125 19317621-6 2009 The results obtained from our Western blots revealed that the cisplatin treatment led to an increase in the level of Bcl-x(L) protein in NF cells, but a decrease in the level of Bcl-x(L) protein in both XPA and XPG cells. Cisplatin 62-71 BCL2 like 1 Homo sapiens 178-186 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 BCL2 like 1 Homo sapiens 99-107 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 BCL2 like 1 Homo sapiens 294-302 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 BCL2 like 1 Homo sapiens 341-349 19414365-10 2009 Our results suggest that the circadian gene Period2 may play an important role in suppression of cell proliferation in human cancer, and additionally Period2 gene expression level may influence the sensitivity to cisplatin depending on Bcl-X(L) expression level. Cisplatin 213-222 BCL2 like 1 Homo sapiens 236-244 19240170-2 2009 EXPERIMENTAL DESIGN: Levels of Bcl-2, Bcl-XL, and Bcl-w were determined and correlated with resistance to cisplatin in a large panel of cell lines derived from squamous cell carcinoma of the head and neck (HNSCC). Cisplatin 106-115 BCL2 like 1 Homo sapiens 38-44 19328230-2 2009 We show here that the DNA-damaging cisplatin-derived anticancer agent oxaliplatin induced both mitochondrial translocation and subsequent Bcl-xL interaction, whereas cisplatin did neither. Cisplatin 35-44 BCL2 like 1 Homo sapiens 138-144 17311906-10 2007 Preincubating cells with the proteasome inhibitor MG-132 or lactacystin not only restored cisplatin-induced loss of Mcl-1 but also resulted in an accumulation of Mcl-1 that exceeded basal levels; however, Bcl-2 and BclxL levels did not change in response to MG-132 or lactacystin. Cisplatin 90-99 BCL2 like 1 Homo sapiens 215-220 18451495-4 2008 Combined treatment with berberine and cisplatin acted in concert to induce loss of mitochondrial membrane potential (Delta Psi m), release of cytochrome-c from mitochondria, and decreased expression of antiapoptotic Bcl-2, Bcl-x/L, resulting in activation of caspases and apoptosis. Cisplatin 38-47 BCL2 like 1 Homo sapiens 223-230 18566236-2 2008 Molecular targeting of Bcl-X(L) and/or Bcl-2 in HNSCC cells has been shown to promote apoptosis signaling and to sensitize cells to chemotherapy drugs, including cisplatin, which is commonly used in the treatment of HNSCC. Cisplatin 162-171 BCL2 like 1 Homo sapiens 23-31 18376141-1 2008 We showed that tumor cells with wild-type p53 and high levels of Bcl-x(L) are cisplatin resistant but are induced to undergo apoptosis by (-)-gossypol, making this a promising agent for overcoming cisplatin resistance. Cisplatin 78-87 BCL2 like 1 Homo sapiens 65-73 18376141-1 2008 We showed that tumor cells with wild-type p53 and high levels of Bcl-x(L) are cisplatin resistant but are induced to undergo apoptosis by (-)-gossypol, making this a promising agent for overcoming cisplatin resistance. Cisplatin 197-206 BCL2 like 1 Homo sapiens 65-73 18376141-3 2008 Conversely, tumor cells with low Bcl-x(L) expression and either wild type or mutant p53 are relatively cisplatin sensitive and do not exhibit such high levels of apoptosis. Cisplatin 103-112 BCL2 like 1 Homo sapiens 33-41 18059167-4 2007 When combined with cisplatin, YC-1 further promoted tumor cell apoptosis, decreased the expression of P-Stat3(705), Bcl-xL, CyclinD1 and survivin, and induced the cleavage of caspase 9 and PARP. Cisplatin 19-28 BCL2 like 1 Homo sapiens 116-122 17619073-7 2007 Similar to function way of SM, cDDP causes cancer cell apoptosis though caspase-8/caspase-3 and Bax/cytochrome c pathways, but the resistance to cDDP is correlated with Bcl-2 and Bcl-xL overexpression. Cisplatin 31-35 BCL2 like 1 Homo sapiens 179-185 17619073-7 2007 Similar to function way of SM, cDDP causes cancer cell apoptosis though caspase-8/caspase-3 and Bax/cytochrome c pathways, but the resistance to cDDP is correlated with Bcl-2 and Bcl-xL overexpression. Cisplatin 145-149 BCL2 like 1 Homo sapiens 179-185 17619073-9 2007 The combined treatment of SM and cDDP significantly reduced Bcl-2 and Bcl-xL expressions, and enhanced Bax, cytochrome c, caspase-9 and -3 expressions in breast cancer cells. Cisplatin 33-37 BCL2 like 1 Homo sapiens 70-76 17399942-7 2007 At 48h, Bax was not up-regulated with any of the treatments, whereas cisplatin was able to induce Bcl-xL down-regulation in both cell lines. Cisplatin 69-78 BCL2 like 1 Homo sapiens 98-104 17399942-17 2007 Cisplatin mechanism of cell death is probably mediated by the decrease in anti-apoptotic protein Bcl-xL whereas paclitaxel and 5FU are decreasing the apoptosis inhibitor survivin. Cisplatin 0-9 BCL2 like 1 Homo sapiens 97-103 17492131-0 2007 Bcl-XL small interfering RNA sensitizes cisplatin-resistant human lung adenocarcinoma cells. Cisplatin 40-49 BCL2 like 1 Homo sapiens 0-6 17383050-8 2007 Targeting of Bcl-xL with siRNA sensitized MPM cells to taurolidine and taurolidine treatment sensitized MPM cells to cisplatin-induced apoptosis. Cisplatin 117-126 BCL2 like 1 Homo sapiens 13-19 17848273-5 2007 RESULTS: HNSCC cell lines selected for cisplatin resistance had wild-type p53 and high levels of Bcl-xL. Cisplatin 39-48 BCL2 like 1 Homo sapiens 97-103 17275076-0 2007 Absence of Bcl-xL down-regulation in response to cisplatin is associated with chemoresistance in ovarian carcinoma cells. Cisplatin 49-58 BCL2 like 1 Homo sapiens 11-17 17275076-2 2007 Our objective was to examine the involvement of Bcl-xL anti-apoptotic protein in resistance to cisplatin. Cisplatin 95-104 BCL2 like 1 Homo sapiens 48-54 17275076-4 2007 We correlated it with Bcl-xL mRNA and protein expression after exposure to cisplatin. Cisplatin 75-84 BCL2 like 1 Homo sapiens 22-28 17275076-8 2007 Wondering whether variation of Bcl-xL level in response to cisplatin could be a better determinant of sensitivity, we investigated the expression of this protein in the cell lines after treatment. Cisplatin 59-68 BCL2 like 1 Homo sapiens 31-37 17275076-9 2007 Cisplatin-induced down-regulation of Bcl-xL was strictly associated with apoptosis and absence of recurrence in vitro. Cisplatin 0-9 BCL2 like 1 Homo sapiens 37-43 17275076-10 2007 Conversely, the maintenance of Bcl-xL expression in response to cisplatin appeared as a sine qua non condition to escape to treatment. Cisplatin 64-73 BCL2 like 1 Homo sapiens 31-37 17848273-6 2007 Expression of wild-type p53 in cell lines with low Bcl-xL enhanced cisplatin sensitivity. Cisplatin 67-76 BCL2 like 1 Homo sapiens 51-57 17848273-7 2007 Expression of both Bcl-xL and wild-type p53 caused tumor cells to become cisplatin resistant. Cisplatin 73-82 BCL2 like 1 Homo sapiens 19-25 17848273-9 2007 Novel agents that inhibit Bcl-xL or activate p53 function may target cisplatin-resistant HNSCC. Cisplatin 69-78 BCL2 like 1 Homo sapiens 26-32 17848273-10 2007 CONCLUSION: Cisplatin resistance in HNSCC is mediated, at least in part, by high Bcl-xL and functional p53. Cisplatin 12-21 BCL2 like 1 Homo sapiens 81-87 16533421-7 2006 Fhit could also partially restore sensitivity to cisplatin in Bcl-2- and Bcl-x(L)-overexpressing H460 cells that are normally resistant to this drug. Cisplatin 49-58 BCL2 like 1 Homo sapiens 73-78 16331250-0 2006 Involvement of Bcl-X(L) deamidation in E1A-mediated cisplatin sensitization of ovarian cancer cells. Cisplatin 52-61 BCL2 like 1 Homo sapiens 15-23 16331250-5 2006 Our data show that cisplatin treatment induced the modification of Bcl-X(L) in the E1A transfectants in dosage and time-dependent manner. Cisplatin 19-28 BCL2 like 1 Homo sapiens 67-75 16331250-10 2006 These findings suggest that Bcl-X(L) deamidation contributes to E1A-mediated cisplatin sensitization in SKOV3.ip1 cells. Cisplatin 77-86 BCL2 like 1 Homo sapiens 28-35 16525642-8 2006 The combination of DHMEQ with cisplatin produced unexpected significant decrease in c-IAP-2 and Bcl-XS mRNAs as well as additive decrease (IL-6, NAIP and, after 16 h, Bcl-XL) or increase (XIAP at 8 h) in gene expression. Cisplatin 30-39 BCL2 like 1 Homo sapiens 167-173 16188300-10 2006 Down-regulation of Bcl-X(L) enhanced the sensitivity of CaOV3, OVCAR3 and SKOV3ip1 to cisplatin and paclitaxel. Cisplatin 86-95 BCL2 like 1 Homo sapiens 19-27 16442262-9 2006 In addition, cisplatin-induced apoptosis is abrogated by the overexpression of either Bcl-2 or Bcl-x(L), which diminished changes of mitochondrial membrane potential and decreased the amount of cytochrome c released from mitochondria. Cisplatin 13-22 BCL2 like 1 Homo sapiens 95-103 16549753-8 2006 RESULTS: There was increased expression of p16, p21, p53, BCLxL, and BCLxS genes with cisplatin treatment in the CCL23 and CCL23AS cells. Cisplatin 86-95 BCL2 like 1 Homo sapiens 58-63 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 BCL2 like 1 Homo sapiens 218-226 16424027-5 2006 The mechanism through which cisplatin achieves these effects is different to daunorubicin and UV light but shows great similarity to the RelA regulatory pathway induced by the ARF tumor suppressor: cisplatin regulation of RelA requires ATR/Chk1 activity, represses Bcl-x(L) but not XIAP expression, and results in phosphorylation of RelA at Thr(505). Cisplatin 28-37 BCL2 like 1 Homo sapiens 265-273 16424027-5 2006 The mechanism through which cisplatin achieves these effects is different to daunorubicin and UV light but shows great similarity to the RelA regulatory pathway induced by the ARF tumor suppressor: cisplatin regulation of RelA requires ATR/Chk1 activity, represses Bcl-x(L) but not XIAP expression, and results in phosphorylation of RelA at Thr(505). Cisplatin 198-207 BCL2 like 1 Homo sapiens 265-273 16020667-7 2005 Thus, cisplatin selected for wild-type p53 and high Bcl-x(L) expression in these cells. Cisplatin 6-15 BCL2 like 1 Homo sapiens 52-60 16115953-9 2005 The attenuation of cisplatin-induced cell death in cyclin D1-overexpressing cells was correlated with the up-regulation of nuclear factor-kappaB activity and maintenance of bcl-2 and bcl-xl protein levels. Cisplatin 19-28 BCL2 like 1 Homo sapiens 183-189 16020667-6 2005 Bcl-x(L) expression increased in the cisplatin-resistant lines relative to the parental lines, whereas Bcl-2 expression was high in the parental lines and decreased in the cisplatin-resistant lines. Cisplatin 37-46 BCL2 like 1 Homo sapiens 0-7 16020667-10 2005 Thus, cisplatin-resistant cells seem to depend on wild-type p53 and Bcl-x(L) for survival and BH3 mimetic agents, such as (-)-gossypol, may be useful adjuncts to overcome cisplatin resistance in HNSCC. Cisplatin 6-15 BCL2 like 1 Homo sapiens 68-76 15958577-2 2005 One of the underlying factors that contribute to cisplatin resistance is the elevated level of BCL-2 and/or BCL-XL, which promotes cell survival. Cisplatin 49-58 BCL2 like 1 Homo sapiens 108-114 15661210-8 2005 We found that Bcl-x(L) expression conferred resistance to chemotherapy-induced apoptosis resulting from treatment with cisplatin, paclitaxel, topotecan, and gemcitabine in vitro. Cisplatin 119-128 BCL2 like 1 Homo sapiens 14-22 15661210-9 2005 In a xenograft model, Bcl-x(L) expressing tumors continued to grow following treatment with cisplatin, paclitaxel, topotecan, and gemcitabine, in contrast to control tumors, which disappeared. Cisplatin 92-101 BCL2 like 1 Homo sapiens 22-30 15566959-11 2004 However, anti-apoptotic Bcl-2 and Bcl-X(L) were elevated and the cell cycle regulator cyclin D1 was slightly upregulated with both 1 and 5 microM cisplatin treatment. Cisplatin 146-155 BCL2 like 1 Homo sapiens 34-42 15156398-8 2004 CONCLUSION: We conclude that overexpression of antiapoptotic proteins Bcl-2 and Bcl-X(L) and down-regulation of caspase-3 activity may be associated with cisplatin resistance in human ovarian cancer. Cisplatin 154-163 BCL2 like 1 Homo sapiens 80-88 15375532-6 2004 In addition, angiotensin II significantly prevented cisplatin (CDDP)-induced apoptosis through NF-kappaB activation and the subsequent production of anti-apoptotic molecules, including survivin and Bcl-XL, in pancreatic cancer cells. Cisplatin 52-61 BCL2 like 1 Homo sapiens 198-204 15375532-6 2004 In addition, angiotensin II significantly prevented cisplatin (CDDP)-induced apoptosis through NF-kappaB activation and the subsequent production of anti-apoptotic molecules, including survivin and Bcl-XL, in pancreatic cancer cells. Cisplatin 63-67 BCL2 like 1 Homo sapiens 198-204 15141012-13 2004 CONCLUSIONS: Exposure of human MPM cells to bcl-xl antisense oligonucleotides sensitizes human mesothelioma cells to the conventional chemotherapeutic agent cisplatin. Cisplatin 157-166 BCL2 like 1 Homo sapiens 44-50 15010843-6 2004 Meanwhile, cisplatin also inhibited Stat3 tyrosine phosphorylation and down-regulated BcL-XL anti-apoptotic protein in the cancer cells tested. Cisplatin 11-20 BCL2 like 1 Homo sapiens 86-92 15026553-8 2004 The level of the anti-apoptotic protein Bcl-x(L) and the pro-apoptotic protein Bax was slightly reduced in H69/CP cells but the ratio of pro-apoptotic and anti-apoptotic Bcl-2 family proteins was not sufficient to explain cellular resistance to cisplatin. Cisplatin 245-254 BCL2 like 1 Homo sapiens 40-48 12667321-1 2002 OBJECTIVE: To investigate the effects of anti-apoptosis gene (bcl-X(L)), cytochrome c and caspase-3 activity on chemoresistance in cisplatin-resistant human ovarian cancer cell lines (A2780/DDP, COC1/DDP). Cisplatin 131-140 BCL2 like 1 Homo sapiens 62-70 15315167-2 2004 Our results showed that (1) "DNA ladder" was observed in A2780 and AD6 after cisplatin treatment; (2) after 3.0, 6.0, 9.9 microg/ml of cisplatin treatment, a significant difference was noted in the rate of apoptosis between in A2780 and AD6 (P<0.05); (3) Bcl-2 and Bcl-xl genes were overexpressed in AD6. Cisplatin 135-144 BCL2 like 1 Homo sapiens 268-274 15315167-3 2004 After cisplatin treatment, the expression of Bcl-2 and Bcl-xl genes was down-regulated in A2780 and AD6. Cisplatin 6-15 BCL2 like 1 Homo sapiens 55-61 15315167-0 2004 Difference in expression of Bcl-2 and Bcl-xl genes in cisplatin-sensitive and cisplatin-resistant human in ovarian cancer cell lines. Cisplatin 54-63 BCL2 like 1 Homo sapiens 38-44 15315167-0 2004 Difference in expression of Bcl-2 and Bcl-xl genes in cisplatin-sensitive and cisplatin-resistant human in ovarian cancer cell lines. Cisplatin 78-87 BCL2 like 1 Homo sapiens 38-44 12950722-10 2003 The combined treatment with genistein and cisplatin significantly reduced bcl-2 and bcl-xL protein and increased Apaf-1 protein expression. Cisplatin 42-51 BCL2 like 1 Homo sapiens 84-90 12536078-6 2003 Cisplatin/Apo2L/TRAIL combination resulted in further downregulation of expression of anti-apoptotic proteins, Bcl-2 and Bcl-xL, as well as an increase in mitochondrial permeability transition and activation of caspases-3, -8, and -10. Cisplatin 0-9 BCL2 like 1 Homo sapiens 121-127 12667321-2 2002 METHODS: The expression of bcl-X(L) cisplatin treated cytochrome c and caspase-3 activity were monitored by RT-PCR and Western blot in cisplatin-resistant (A2780/DDP, COC1/DDP) and cisplatin-sensitive (A2780, COC1) cell lines. Cisplatin 36-45 BCL2 like 1 Homo sapiens 27-35 12667321-2 2002 METHODS: The expression of bcl-X(L) cisplatin treated cytochrome c and caspase-3 activity were monitored by RT-PCR and Western blot in cisplatin-resistant (A2780/DDP, COC1/DDP) and cisplatin-sensitive (A2780, COC1) cell lines. Cisplatin 135-144 BCL2 like 1 Homo sapiens 27-35 12667321-2 2002 METHODS: The expression of bcl-X(L) cisplatin treated cytochrome c and caspase-3 activity were monitored by RT-PCR and Western blot in cisplatin-resistant (A2780/DDP, COC1/DDP) and cisplatin-sensitive (A2780, COC1) cell lines. Cisplatin 135-144 BCL2 like 1 Homo sapiens 27-35 12667321-4 2002 RESULTS: The expression of bcl-X(L) in A2780/DDP and COC1/DDP was significantly higher than that in A2780 and COC1 cells, whereas the expression of cytochrome c, caspase-3 activity and apoptotic rates of A2780/DDP and COC1/DDP were significantly reduced more than those of A2780 and COC1 after having been treated by cisplatin (P < 0.05). Cisplatin 317-326 BCL2 like 1 Homo sapiens 27-35 12667321-5 2002 CONCLUSION: The overexpression of anti-apoptotic gene bcl-X(L), which downregulates cytochrome c and decreases caspase-3 activity, may be related to cisplatin-resistance in human ovarian cancer cell lines. Cisplatin 149-158 BCL2 like 1 Homo sapiens 54-62 11948488-5 2002 Overexpression of Bcl-x(L) in stably transfected human melanoma Mel Juso cells significantly reduced sensitivity to cisplatin-induced apoptosis (p < or = 0.05). Cisplatin 116-125 BCL2 like 1 Homo sapiens 18-26 11857368-1 2002 The effect of overexpressing the antiapoptotic protein BclXL in a human ovarian carcinoma cell line has been investigated in terms of sensitivity to the 2 major drugs used to treat this disease, paclitaxel and cisplatin. Cisplatin 210-219 BCL2 like 1 Homo sapiens 55-60 11857368-2 2002 Stable transfection of BclXL into CH1 cells, which are relatively sensitive to cisplatin, resulted in around 2.7-fold higher expression in comparison with empty vector controls. Cisplatin 79-88 BCL2 like 1 Homo sapiens 23-28 11857368-4 2002 By contrast, parallel subcutaneous xenograft models of these isogenic ovarian carcinoma cells in vivo, differing only in BclXL status, showed that this low-level BclXL overexpression conferred significant resistance to both paclitaxel and cisplatin in comparison with parent, nontransfected tumours. Cisplatin 239-248 BCL2 like 1 Homo sapiens 162-167 11857368-7 2002 These data suggest that the responsiveness of ovarian cancer to paclitaxel and cisplatin in vivo, and therefore perhaps clinically, is influenced by levels of the antiapoptotic protein BclXL. Cisplatin 79-88 BCL2 like 1 Homo sapiens 185-190 11368186-2 2001 The present study revealed that administration of cis-diamminedichloroplatinum(II)-elicited oxidative stress in renal mitochondria, decreased the renal expression of Bcl-x, released cytochrome c from mitochondria to cytosol, and induced apoptosis and renal dysfunction by a mechanism that was inhibited by AH-SOD. Cisplatin 50-82 BCL2 like 1 Homo sapiens 166-171 11734333-6 2002 With cisplatin at a high dose, both cell lines underwent apoptosis that was accompanied by downregulation of p27(KIP1) and Bcl-x(L). Cisplatin 5-14 BCL2 like 1 Homo sapiens 123-131 11384107-9 2001 Expression of Bcl-xL decreased after exposure to CDDP in SK-OV-3 cells with and without transduction. Cisplatin 49-53 BCL2 like 1 Homo sapiens 14-20 10397248-8 1999 Bcl-2 and Bcl-xL proteins remained relatively unchanged in expression for over 48 h after exposure to cisplatin in the A2780 cell lines. Cisplatin 102-111 BCL2 like 1 Homo sapiens 10-16 10974635-5 2000 After exposure to CDDP, p53 and Bax protein expression increased and Bcl-xL expression decreased in the KF cells and TP53 gene-transducted SK-OV-3 cells. Cisplatin 18-22 BCL2 like 1 Homo sapiens 69-75 9393748-2 1997 Here, we demonstrate that expression of galectin-3 in human breast carcinoma BT549 cells inhibits cis-diamminedichloroplatinum (cisplatin)-induced poly(ADP-ribose) polymerase degradation and apoptosis, without altering Bcl-2, Bcl-X(L), or Bax expressions. Cisplatin 128-137 BCL2 like 1 Homo sapiens 226-234 9790794-12 1998 Bcl-xL-expressing cells were highly resistant to cisplatin and Taxol compared with controls (P < 0.05). Cisplatin 49-58 BCL2 like 1 Homo sapiens 0-6 9642215-2 1998 The present studies demonstrate that SCC-25 cells selected for resistance to the alkylating agent cisplatin (CDDP) overexpress the anti-apoptotic Bcl-xL protein. Cisplatin 98-107 BCL2 like 1 Homo sapiens 146-152 9642215-2 1998 The present studies demonstrate that SCC-25 cells selected for resistance to the alkylating agent cisplatin (CDDP) overexpress the anti-apoptotic Bcl-xL protein. Cisplatin 109-113 BCL2 like 1 Homo sapiens 146-152 9576951-4 1998 Expression of Bcl-XL was elevated in U87MG.DeltaEGFR cells prior to and during CDDP treatment, whereas it decreased considerably in CDDP-treated parental cells. Cisplatin 79-83 BCL2 like 1 Homo sapiens 14-20 9576951-4 1998 Expression of Bcl-XL was elevated in U87MG.DeltaEGFR cells prior to and during CDDP treatment, whereas it decreased considerably in CDDP-treated parental cells. Cisplatin 132-136 BCL2 like 1 Homo sapiens 14-20 9576951-8 1998 Ectopic overexpression of Bcl-XL in parental U87MG cells also resulted in suppression of both caspase activation and apoptosis induced by CDDP. Cisplatin 138-142 BCL2 like 1 Homo sapiens 26-32 9570926-5 1998 Modulation of cell death by Bcl-xL was also observed in cells treated with etoposide, vinblastine, paclitaxel, and cisplatinum (II) diammine dichloride. Cisplatin 115-126 BCL2 like 1 Homo sapiens 28-34 7655019-4 1995 Bcl-XL expression dramatically reduces the cytotoxicity of bleomycin, cisplatin, etoposide, vincristine, hygromycin B, and mycophenolic acid for up to 4 days in culture. Cisplatin 70-79 BCL2 like 1 Homo sapiens 0-6 14646525-6 1997 Stable transfection of U2-OS cells with bcl-xL cDNA conferred a low level of drug resistance to cisplatin, suggesting that overexpression of this gene contributes to the cisplatin-resistant phenotype of this osteosarcoma cell system. Cisplatin 96-105 BCL2 like 1 Homo sapiens 40-46 14646525-6 1997 Stable transfection of U2-OS cells with bcl-xL cDNA conferred a low level of drug resistance to cisplatin, suggesting that overexpression of this gene contributes to the cisplatin-resistant phenotype of this osteosarcoma cell system. Cisplatin 170-179 BCL2 like 1 Homo sapiens 40-46 8798452-0 1996 Bax can antagonize Bcl-XL during etoposide and cisplatin-induced cell death independently of its heterodimerization with Bcl-XL. Cisplatin 47-56 BCL2 like 1 Homo sapiens 19-25 8798452-4 1996 Expression of wild-type Bax countered the repressor activity of Bcl-XL against cell death mediated by VP-16 and cisplatin. Cisplatin 112-121 BCL2 like 1 Homo sapiens 64-70 9494534-9 1997 Expression of bcl-2 family members (bax, bcl-x) was modulated by fotemustine, etoposide and cisplatin. Cisplatin 92-101 BCL2 like 1 Homo sapiens 41-46 34907000-8 2022 BCL-XL inhibitors such as ABT-263 (Navitoclax) have the capacity to be used in combination with cisplatin in head and neck cancer patients to eliminate senescent cells and possibly prevent disease relapse. Cisplatin 96-105 BCL2 like 1 Homo sapiens 0-6 22033921-9 2011 We found that PCMT1 silencing is associated with an increase of the BclxL isoform reported to be inactivated by deamidation, thus making cells more susceptible to apoptosis induced by cisplatinum. Cisplatin 184-195 BCL2 like 1 Homo sapiens 68-73 34111459-0 2021 Bcl-xL expression and regulation in the progression, recurrence, and cisplatin resistance of oral cancer. Cisplatin 69-78 BCL2 like 1 Homo sapiens 0-6 34111459-9 2021 CONCLUSION: Collectively, we have demonstrated the role of Bcl-xL and AP-1 (Fra-2), causing OSCC progression and cisplatin resistance. Cisplatin 113-122 BCL2 like 1 Homo sapiens 59-65 32945500-9 2020 The combination treatment of cisplatin and ECL promoted cell apoptosis more effectively than cisplatin alone, as revealed by the increased cleaved caspase-3, but decreased Bcl-xL and survivin levels. Cisplatin 29-38 BCL2 like 1 Homo sapiens 172-178 34088830-7 2021 DBP predicted that targeting either Mcl-1 or Bcl-xL increases the efficacy of the chemotherapeutic agent, cisplatin, whereas targeting Bcl-2 does not. Cisplatin 106-115 BCL2 like 1 Homo sapiens 45-51 34322387-11 2021 Conclusion: Downregulation of ATXN3 enhanced AKT inhibitors (perifosine or MK-2206) induced cell death by BIM, but decreased the cell death induced by chemotherapeutic drugs (etoposide or cisplatin) via Bcl-xl. Cisplatin 188-197 BCL2 like 1 Homo sapiens 203-209 32881195-5 2021 Moreover, the elevation of apoptosis including Bax, Bad, cleaved caspase-3,-9, and decreased protein levels of Bcl-2, Bcl-XL induced by cisplatin were reversed after PD treatment. Cisplatin 136-145 BCL2 like 1 Homo sapiens 118-124 30032449-10 2018 Using the UMUC-3 cells stably depleted of endogenous GRIM19, we further show that inhibition of Bcl-xL rectified GRIM19 deficiency-caused CDDP resistance in BC cells. Cisplatin 138-142 BCL2 like 1 Homo sapiens 96-102 31648572-7 2020 Abbreviations AKT protein kinase B ARMS alveolar rhabdomyosarcoma ATM ataxia telangiectasia mutated Bax Bcl-2-associated X protein Bcl-2 B-cell lymphoma 2 CDC2 cyclin-dependent kinase 2 Bcl-xL B-cell lymphoma-extra large c-FLIP cellular FLICE-like inhibitory protein CDDP cisplatin COX-2 cyclooxygenase-2 cyt c cytochrome c DNA-PKcs DNA-dependent protein kinase EGFR epidermal growth factor receptor EMT epithelial-mesenchymal transition ERK extracellular signal-regulated kinase ES Ewing`s sarcoma ETS2 erythroblastosis virus transcription factor 2 GBM glioblastoma multiforme HCC hepatocellular carcinoma HNSCC head and neck squamous cell carcinoma IAP inhibitor of apoptosis protein IkappaBalpha inhibitor of kappaB alpha IKK inhibitor of kappaB kinase IR ionizing radiation lncRNA long non-coding RNA luc luciferase Mcl-1 myeloid cell leukemia-1 MDR1 multidrug resistance protein 1 miR microRNA MMP-9 matrix metalloproteinase-9 mTOR mammalian target of rapamycin NB neuroblastoma NF-kappaB nuclear factor-kappaB NPC nasopharyngeal carcinoma NSCLC non-small cell lung cancer OSCC oral squamous cell carcinoma PARP poly-(ADP-ribose)-polymerase pH2AX phosphorylated histone 2AX-immunoreactive PI3K phosphatidylinositol 3-kinase Prp4K Pre-mRNA processing factor 4 kinase RCC renal cell carcinoma ROS reactive oxygen species SCC squamous cell carcinoma SLN solid lipid nanoparticle SOD2 superoxide dismutase 2 TERT telomerase reverse transcriptase TNF-alpha tumor necrosis factor-alpha TxnRd1 thioredoxin reductase-1 VEGF vascular endothelial growth factor XIAP X-linked inhibitor of apoptosis protein DeltaPsim mitochondrial membrane potential. Cisplatin 267-281 BCL2 like 1 Homo sapiens 186-192 31462500-8 2019 Conversely, specific inhibitors of BCL-XL, MCL1, or BCL-XL/BCL-2, but not BCL-2 alone, enhanced cell death when combined with cisplatin or paclitaxel. Cisplatin 126-135 BCL2 like 1 Homo sapiens 35-41 31462500-8 2019 Conversely, specific inhibitors of BCL-XL, MCL1, or BCL-XL/BCL-2, but not BCL-2 alone, enhanced cell death when combined with cisplatin or paclitaxel. Cisplatin 126-135 BCL2 like 1 Homo sapiens 52-58 31754340-5 2019 Western blot showed that in intrinsic apoptosis induced by cisplatin, the overexpression of RMP promoted the Bcl-xl expression both in vitro and in vivo. Cisplatin 59-68 BCL2 like 1 Homo sapiens 109-115 31262032-6 2019 Our results revealed that cisplatin-resistant UC cells (T24/R) upregulated the antiapoptotic factor, B-cell lymphoma-extra large (Bcl-xL). Cisplatin 26-35 BCL2 like 1 Homo sapiens 130-136 31262032-7 2019 Knockdown of Bcl-xL by siRNA resensitized cisplatin-resistant cells to the cisplatin cytotoxic effect. Cisplatin 42-51 BCL2 like 1 Homo sapiens 13-19 31262032-7 2019 Knockdown of Bcl-xL by siRNA resensitized cisplatin-resistant cells to the cisplatin cytotoxic effect. Cisplatin 75-84 BCL2 like 1 Homo sapiens 13-19 30032449-12 2018 CONCLUSIONS: Disruption of GRIM19/Bcl-xL is a key mechanism of CDDP resistance in advanced BC. Cisplatin 63-67 BCL2 like 1 Homo sapiens 34-40 28963947-5 2017 Here, we report that the BCL2/BCLXL inhibitor ABT737 induced apoptosis more potently in cisplatin-resistant SKOV3/DDP ovarian cancer cells than in cisplatin-sensitive SKOV3 ovarian cancer cells. Cisplatin 88-97 BCL2 like 1 Homo sapiens 30-35 29203930-7 2018 The expression levels of Bax and Cyt-c proteins were upregulated, but the expression levels of Bcl-2 and Bcl-xL proteins were downregulated by blocking CDH17 gene in gastric cancer BGC823 cells after treatment with cisplatin. Cisplatin 215-224 BCL2 like 1 Homo sapiens 105-111 29352235-8 2018 In silico predictions by DR_MOMP revealed substantial differences in treatment responses of BCL(X)L, BCL2 or MCL1 inhibitors combinations with cisplatin that were successfully validated in cell lines. Cisplatin 143-152 BCL2 like 1 Homo sapiens 92-99 28597042-1 2017 PURPOSE: Change of multidrug resistance-related genes (e.g., lung resistance protein, LRP) and overexpression of anti-apoptotic genes (Bcl-2, Bcl-Xl, XIAP, Survivin) are responsible for cisplatin resistance. Cisplatin 186-195 BCL2 like 1 Homo sapiens 142-148 29262633-10 2017 Since Bcl-xl is a key anti-apoptotic protein, we found that sensitivity of NSCLC cells to cisplatin-induced apoptosis was significantly increased because of the overexpression of miR-216b. Cisplatin 90-99 BCL2 like 1 Homo sapiens 6-12 28979680-10 2017 After treatment of cisplatin, SKOV3 and hey cells showed increased apoptotic rate in flow cytometry assay, increased protein levels of cleaved caspase 3, cleaved PARP and Bax, and decreased protein levels of Bcl-2 and Bcl-XL. Cisplatin 19-28 BCL2 like 1 Homo sapiens 218-224 28597042-2 2017 In our study, we investigated the mechanism by which cisplatin induces LRP, Bcl-2, Bcl-xL, XIAP, and Survivin expression in human lung adenocarcinoma A549 cells and human H446 small cell lung cancer cells at mRNA and protein levels. Cisplatin 53-62 BCL2 like 1 Homo sapiens 83-89 28597042-6 2017 RESULTS: Cisplatin increased Bcl-2, LRP, and Survivin expression, but decreased Bcl-xL and XIAP expression in a dose-dependent manner. Cisplatin 9-18 BCL2 like 1 Homo sapiens 80-86 27127878-0 2016 FXR agonists enhance the sensitivity of biliary tract cancer cells to cisplatin via SHP dependent inhibition of Bcl-xL expression. Cisplatin 70-79 BCL2 like 1 Homo sapiens 112-118 28617432-7 2017 Further investigation demonstrated that BST2-mediated cisplatin resistance depended on the activation of the NF-kappaB signaling pathway and consequent upregulation of anti-apoptotic genes, such as Bcl-XL and livin. Cisplatin 54-63 BCL2 like 1 Homo sapiens 198-204 27015836-5 2016 After knockdown of Nrf2, the sensitivity of those cells to the cytotoxicity of cisplatin (Cis) was enhanced in association with the increased release of AIF and downregulation of Bcl-xl in both cells. Cisplatin 79-88 BCL2 like 1 Homo sapiens 179-185 27494891-6 2016 Mechanistic studies suggested that treatment of cells with PHPO or with PHPO + cisplatin differentially inhibited the PI3K/Akt, MAPK and ATM/Chk2 pathways, which consequently suppressed the anti-apoptotic factors Bcl-xL, Bcl-2 and XIAP, but activated the pro-apoptotic factors Bad, Bax, p53, caspase 9, caspase 8, caspase 7 and PARP. Cisplatin 79-88 BCL2 like 1 Homo sapiens 213-219 27127878-5 2016 Mechanistically, we found that activation of FXR induced expression of small heterodimer partner (SHP), which in turn inhibited signal transducer and activator of transcription 3 (STAT3) phosphorylation and resulted in down-regulation of Bcl-xL expression in BTC cells, leading to increased susceptibility to CDDP. Cisplatin 309-313 BCL2 like 1 Homo sapiens 238-244 26860078-0 2016 beta-Catenin signaling pathway regulates cisplatin resistance in lung adenocarcinoma cells by upregulating Bcl-xl. Cisplatin 41-50 BCL2 like 1 Homo sapiens 107-113 26860078-13 2016 The findings of the current study suggest that upregulation of beta-catenin signaling may contribute to cisplatin resistance in lung adenocarcinoma cells by upregulating Bcl-xl. Cisplatin 104-113 BCL2 like 1 Homo sapiens 170-176 25992654-10 2015 These findings demonstrate that MEG3 is significantly downregulated in LAD and partially regulates the cisplatin resistance of LAD cells through the control of p53 and Bcl-xl expression. Cisplatin 103-112 BCL2 like 1 Homo sapiens 168-174 27226901-4 2016 We show that the chemotherapeutic drug cisplatin initiates an apoptotic pathway by phosphorylation of a pro-survival Bcl-2 family member, Bcl-xL, by cyclin-dependent kinase 2. Cisplatin 39-48 BCL2 like 1 Homo sapiens 138-144 27226901-5 2016 The phosphorylation occurred at a previously unreported site and its biologic significance was demonstrated by a phosphomimetic modification of Bcl-xL that was able to induce apoptosis without addition of cisplatin. Cisplatin 205-214 BCL2 like 1 Homo sapiens 144-150 26239225-0 2015 MicroRNA-133a and microRNA-326 co-contribute to hepatocellular carcinoma 5-fluorouracil and cisplatin sensitivity by directly targeting B-cell lymphoma-extra large. Cisplatin 92-101 BCL2 like 1 Homo sapiens 136-163 26239225-9 2015 The results of the present study indicated that miR-133a, miR-326 and Bcl-xl acted protectively against the apoptosis, induced by 5-FU or DDP, in HepG2 cells. Cisplatin 138-141 BCL2 like 1 Homo sapiens 70-76 26201840-12 2015 In combinatory treatments, the Bcl-xL-directed siRNA markedly enhanced the anti-proliferative and apoptotic effects of CDDP and therefore, may serve as suitable tool for chemosensitization of BCa cells. Cisplatin 119-123 BCL2 like 1 Homo sapiens 31-37 26497680-6 2015 Among the Nrf2 downstream genes, Bcl-2 and Bcl-xL contribute more strongly to Nrf2-mediated cisplatin resistance when compared with heme oxygenase 1 (HO-1). Cisplatin 92-101 BCL2 like 1 Homo sapiens 43-49 26497680-7 2015 Cox regression analysis showed that patients with high-Nrf2, high-Bcl-2, high-Bcl-xL mRNA tumors were more commonly occurred unfavorable response to cisplatin-based chemotherapy than their counterparts. Cisplatin 149-158 BCL2 like 1 Homo sapiens 78-84 26592553-0 2015 MLN4924 Synergistically Enhances Cisplatin-induced Cytotoxicity via JNK and Bcl-xL Pathways in Human Urothelial Carcinoma. Cisplatin 33-42 BCL2 like 1 Homo sapiens 76-82 26592553-6 2015 c-Jun N-terminal kinase (JNK) activation and a down-regulation of B-cell lymphoma-extra large (Bcl-xL) were also observed during cisplatin and MLN4924 treatment. Cisplatin 129-138 BCL2 like 1 Homo sapiens 95-101 26592553-10 2015 In summary, MLN4924 synergistically enhanced the anti-tumor effect of cisplatin via an increase in DNA damage, JNK activation and down-regulation of Bcl-xL in urothelial carcinoma cells. Cisplatin 70-79 BCL2 like 1 Homo sapiens 149-155 25310746-0 2015 The alkaloid emetine sensitizes ovarian carcinoma cells to cisplatin through downregulation of bcl-xL. Cisplatin 59-68 BCL2 like 1 Homo sapiens 95-101 25310746-7 2015 As to the mechanism, downregulation of bcl-xL by emetine was shown to be responsible for enhancing the sensitivity of ovarian cancer cells to cisplatin. Cisplatin 142-151 BCL2 like 1 Homo sapiens 39-45 24286513-6 2014 Genes displaying increase in expression of apoptosis, related to cisplatin treatment, were Casp8, Bcl10, Bcl2, Bcl2l1, Bcl2l2, Bid, Naip1, Bnip3l, Card6, Pak7, Cd40, Trp 53inp1, Cideb and Cd70. Cisplatin 65-74 BCL2 like 1 Homo sapiens 111-117 24637722-9 2014 We also found that CCN2 provided resistance to cisplatin-induced apoptosis through upregulation of Bcl-xL and survivin. Cisplatin 47-56 BCL2 like 1 Homo sapiens 99-105 24637722-10 2014 Knockdown of Bcl-xL or survivin removed the CCN2-mediated resistance to apoptosis induced by cisplatin. Cisplatin 93-102 BCL2 like 1 Homo sapiens 13-19 24400442-0 2013 Let-7c sensitizes acquired cisplatin-resistant A549 cells by targeting ABCC2 and Bcl-XL. Cisplatin 27-36 BCL2 like 1 Homo sapiens 81-87 23027129-6 2013 Silencing of FGFR2 sensitized NB cells to cisplatin-induced apoptosis, which was regulated by the downregulation of the anti-apoptotic proteins BCL2 and BCLXL. Cisplatin 42-51 BCL2 like 1 Homo sapiens 153-158 23912708-9 2013 Moreover, the induction of apoptosis by TRAIL plus cisplatin was accompanied by the downregulation of cFLIP and BCL2L1, and simultaneously robust enzymatic activation of caspase-8, culminating in decreased cancer cell survival. Cisplatin 51-60 BCL2 like 1 Homo sapiens 112-118 23969971-5 2013 Early in the time course of drug administration, cisplatin increased the expression of pSTAT3 (Tyr705), STAT3alpha, VEGF, survivin, and Bcl-XL, while oxaliplatin and nedaplatin exhibited the opposite effects, and upregulated pSTAT3 (Ser727) and STAT3beta. Cisplatin 49-58 BCL2 like 1 Homo sapiens 136-142