PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10353733-2 1999 We investigated the response of the mitogen-activated protein kinases, extracellular signal-regulated kinases 1 and 2 (ERK1/2), c-Jun-N-terminal kinase 1 (JNK1), and p38, to cisplatin treatment in the ovarian carcinoma cell line SK-OV-3. Cisplatin 174-183 mitogen-activated protein kinase 8 Homo sapiens 155-159 10353733-2 1999 We investigated the response of the mitogen-activated protein kinases, extracellular signal-regulated kinases 1 and 2 (ERK1/2), c-Jun-N-terminal kinase 1 (JNK1), and p38, to cisplatin treatment in the ovarian carcinoma cell line SK-OV-3. Cisplatin 174-183 mitogen-activated protein kinase 8 Homo sapiens 128-153 10353733-3 1999 Cisplatin caused a late and prolonged induction in a dose-dependent manner of both ERK1/2 and JNK1 activity. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 94-98 10353733-4 1999 ERK1/2 and JNK1 activities continued to increase in magnitude up to 24 h following initiation of cisplatin treatment. Cisplatin 97-106 mitogen-activated protein kinase 8 Homo sapiens 11-15 10098743-0 1999 Induction of JNK and c-Abl signalling by cisplatin and oxaliplatin in mismatch repair-proficient and -deficient cells. Cisplatin 41-50 mitogen-activated protein kinase 8 Homo sapiens 13-16 10098743-3 1999 To identify the signal transduction pathways with which the detector communicates, we investigated the effect of loss of DNA mismatch repair on activation of known damage-responsive pathways, and recently reported that cisplatin differentially activates c-Jun NH2-terminal kinase (JNK) and c-Abl in repair-proficient vs.-deficient cells. Cisplatin 219-228 mitogen-activated protein kinase 8 Homo sapiens 254-279 10098743-3 1999 To identify the signal transduction pathways with which the detector communicates, we investigated the effect of loss of DNA mismatch repair on activation of known damage-responsive pathways, and recently reported that cisplatin differentially activates c-Jun NH2-terminal kinase (JNK) and c-Abl in repair-proficient vs.-deficient cells. Cisplatin 219-228 mitogen-activated protein kinase 8 Homo sapiens 281-284 9162025-1 1997 We have studied the role of Jun/stress-activated protein kinase (JNK/SAPK) pathway in DNA repair and cisplatin resistance in T98G glioblastoma cells. Cisplatin 101-110 mitogen-activated protein kinase 8 Homo sapiens 65-73 10098743-5 1999 The results confirm that cisplatin activates JNK kinase 5.7 +/- 1.5 (s.d. Cisplatin 25-34 mitogen-activated protein kinase 8 Homo sapiens 45-48 10098743-9 1999 The DNA mismatch repair system plays an important part in the recognition of cisplatin adducts, and activation of both the JNK and c-Abl kinases in response to cisplatin damage is dependent on the detector function of the DNA mismatch repair proteins. Cisplatin 77-86 mitogen-activated protein kinase 8 Homo sapiens 123-126 10098743-9 1999 The DNA mismatch repair system plays an important part in the recognition of cisplatin adducts, and activation of both the JNK and c-Abl kinases in response to cisplatin damage is dependent on the detector function of the DNA mismatch repair proteins. Cisplatin 160-169 mitogen-activated protein kinase 8 Homo sapiens 123-126 9926932-2 1999 In this study, we found that the DNA-damaging agent cisplatin (cDDP) activated MAP kinase kinase kinase ASK1 and subsequent downstream subgroups of MAP kinase kinase, SEK1 (or MKK4) and MKK3/MKK6, which in turn activated c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK) and p38 MAP kinase prior to caspase family protease activation and the onset of apoptosis in human ovarian carcinoma (OVCAR-3) and human kidney (293T) cells. Cisplatin 52-61 mitogen-activated protein kinase 8 Homo sapiens 280-284 9926932-2 1999 In this study, we found that the DNA-damaging agent cisplatin (cDDP) activated MAP kinase kinase kinase ASK1 and subsequent downstream subgroups of MAP kinase kinase, SEK1 (or MKK4) and MKK3/MKK6, which in turn activated c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK) and p38 MAP kinase prior to caspase family protease activation and the onset of apoptosis in human ovarian carcinoma (OVCAR-3) and human kidney (293T) cells. Cisplatin 63-67 mitogen-activated protein kinase 8 Homo sapiens 280-284 10081494-8 1998 Since CDDP and carboplatin damage DNA and then activate c-abl and the JNK/SAPK pathway, EAT/mcl-1 may inhibit p53-independent apoptosis through a c-abl/JNK (SAPK)-dependent mechanism. Cisplatin 6-10 mitogen-activated protein kinase 8 Homo sapiens 70-73 10081494-8 1998 Since CDDP and carboplatin damage DNA and then activate c-abl and the JNK/SAPK pathway, EAT/mcl-1 may inhibit p53-independent apoptosis through a c-abl/JNK (SAPK)-dependent mechanism. Cisplatin 6-10 mitogen-activated protein kinase 8 Homo sapiens 152-155 9484843-0 1998 Cisplatin induces a persistent activation of JNK that is related to cell death. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 45-48 9484843-10 1998 The positive modulation of JNK activation correlates with an increase in toxicity that, for cis-DDP corresponds to a tenfold decrease in the IC50. Cisplatin 92-99 mitogen-activated protein kinase 8 Homo sapiens 27-30 9484843-12 1998 Altogether the results suggest that the prolonged activation of JNK in response to cis-DDP contributes to cell death induction. Cisplatin 83-90 mitogen-activated protein kinase 8 Homo sapiens 64-67 9242457-1 1997 The c-Abl nonreceptor tyrosine kinase and the c-Jun NH2-terminal kinase (JNK/stress-activated protein kinase) are activated during the injury response to the DNA-damaging agent cisplatin. Cisplatin 177-186 mitogen-activated protein kinase 8 Homo sapiens 73-76 9242457-3 1997 To identify signaling pathways activated by this detector, we investigated the effect of the loss of DNA mismatch repair function on the ability of cisplatin to activate the JNK and c-Abl kinases. Cisplatin 148-157 mitogen-activated protein kinase 8 Homo sapiens 174-177 9242457-4 1997 The results demonstrate that cisplatin activates JNK kinase 3.8 +/- 0.2-fold more efficiently in DNA mismatch repair-proficient than repair-deficient cells, and that activation of c-Abl is completely absent in the DNA mismatch repair-deficient cells. Cisplatin 29-38 mitogen-activated protein kinase 8 Homo sapiens 49-52 9242457-5 1997 Furthermore, the results show that cisplatin-induced activation of JNK occurs through a stress-activated protein kinase/extracellular signal-regulated kinase kinase 1-independent mechanism. Cisplatin 35-44 mitogen-activated protein kinase 8 Homo sapiens 67-70 9242457-6 1997 We conclude that activation of JNK and c-Abl by cisplatin is in part dependent upon the integrity of DNA mismatch repair function, suggesting that these kinases are part of the signal transduction pathway activated when mismatch repair proteins recognize cisplatin adducts in DNA. Cisplatin 48-57 mitogen-activated protein kinase 8 Homo sapiens 31-34 9242457-6 1997 We conclude that activation of JNK and c-Abl by cisplatin is in part dependent upon the integrity of DNA mismatch repair function, suggesting that these kinases are part of the signal transduction pathway activated when mismatch repair proteins recognize cisplatin adducts in DNA. Cisplatin 255-264 mitogen-activated protein kinase 8 Homo sapiens 31-34 9252645-7 1997 Finally, we show that cisplatin causes only weak activation of Jun N-terminal kinase (JNK) in a human melanoma cell line. Cisplatin 22-31 mitogen-activated protein kinase 8 Homo sapiens 63-84 9252645-7 1997 Finally, we show that cisplatin causes only weak activation of Jun N-terminal kinase (JNK) in a human melanoma cell line. Cisplatin 22-31 mitogen-activated protein kinase 8 Homo sapiens 86-89 9162025-3 1997 We show that treatment of T98G glioblastoma cells with cisplatin but not the transplatin isomer activates JNK/SAPK about 10-fold. Cisplatin 55-64 mitogen-activated protein kinase 8 Homo sapiens 106-109 9162025-8 1997 These observations indicate that the JNK/SAPK pathway is activated by cisplatin-induced DNA damage and that this response is required for DNA repair and viability following cisplatin treatment. Cisplatin 70-79 mitogen-activated protein kinase 8 Homo sapiens 37-40 9162025-8 1997 These observations indicate that the JNK/SAPK pathway is activated by cisplatin-induced DNA damage and that this response is required for DNA repair and viability following cisplatin treatment. Cisplatin 173-182 mitogen-activated protein kinase 8 Homo sapiens 37-40 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 mitogen-activated protein kinase 8 Homo sapiens 89-92 33973461-6 2021 Moreover, OPZ promoted the phosphorylation of the apoptosis signaling pathway JNK that was activated by cisplatin, thereby inducing tumor cell apoptosis. Cisplatin 104-113 mitogen-activated protein kinase 8 Homo sapiens 78-81 34533242-7 2021 Biochemical experiments further discovered that rosamultin could inhibit p38 and JNK activation, and downregulate the levels of CHOP and proteins in its upstream PERK-eIF2alpha-ATF4 signaling pathway stimulated by cisplatin or tunicamycin. Cisplatin 214-223 mitogen-activated protein kinase 8 Homo sapiens 81-84 34274415-6 2021 Our results demonstrated that cisplatin concurrently induced apoptosis and autophagy in OSCC cell lines partially through the ROS/JNK pathway. Cisplatin 30-39 mitogen-activated protein kinase 8 Homo sapiens 130-133 35578316-14 2022 The enhancement of the effect of cisplatin according to SCARA3 overexpression is via the AKT and JNK pathways. Cisplatin 33-42 mitogen-activated protein kinase 8 Homo sapiens 97-100 34306367-0 2021 CHOP overexpression sensitizes human non-small cell lung cancer cells to cisplatin treatment by Bcl-2/JNK pathway. Cisplatin 73-82 mitogen-activated protein kinase 8 Homo sapiens 102-105 34306367-7 2021 CHOP increased the therapeutic effect of cisplatin on NSCLC cells through the Bcl-2/JNK pathway. Cisplatin 41-50 mitogen-activated protein kinase 8 Homo sapiens 84-87 34306367-8 2021 In summary, CHOP regulated cisplatin resistance in cells of NSCLC by promoting the expression of apoptotic proteins and inhibiting the Bcl-2/JNK signaling pathway, indicating the antitumor effects of CHOP. Cisplatin 27-36 mitogen-activated protein kinase 8 Homo sapiens 141-144 35001794-11 2022 It protected HK-2 cells from cisplatin-induced apoptosis by targeting and down-regulating the mitogen-activated protein kinase 8 (MAPK8). Cisplatin 29-38 mitogen-activated protein kinase 8 Homo sapiens 94-128 35179434-0 2022 Circ_0067934 reduces JNK phosphorylation through a microRNA-545-3p/PPA1 axis to enhance tumorigenesis and cisplatin resistance in ovarian cancer. Cisplatin 106-115 mitogen-activated protein kinase 8 Homo sapiens 21-24 35236965-7 2022 Furthermore, STAMBPL1 and MKP-1 depletion increased breast cancer sensitivity to cisplatin by increasing the phosphorylation and activation of c-Jun N-terminal protein kinase (JNK). Cisplatin 81-90 mitogen-activated protein kinase 8 Homo sapiens 143-174 35236965-7 2022 Furthermore, STAMBPL1 and MKP-1 depletion increased breast cancer sensitivity to cisplatin by increasing the phosphorylation and activation of c-Jun N-terminal protein kinase (JNK). Cisplatin 81-90 mitogen-activated protein kinase 8 Homo sapiens 176-179 35251480-9 2022 Mechanistically, we found that GLB enhances the sensitivity of ovarian cancer cells to cisplatin via increasing reactive oxygen species (ROS) levels, the phosphorylation of c-Jun N-terminal kinase (JNK), and DNA damage. Cisplatin 87-96 mitogen-activated protein kinase 8 Homo sapiens 173-196 35251480-9 2022 Mechanistically, we found that GLB enhances the sensitivity of ovarian cancer cells to cisplatin via increasing reactive oxygen species (ROS) levels, the phosphorylation of c-Jun N-terminal kinase (JNK), and DNA damage. Cisplatin 87-96 mitogen-activated protein kinase 8 Homo sapiens 198-201 35001794-12 2022 Together, our findings identified that the urinary exosomes derived from premature infants alleviated cisplatin-induced acute kidney injury and inhibited the apoptosis of HK-2 via miR-30a-5p, which could target MAPK8. Cisplatin 102-111 mitogen-activated protein kinase 8 Homo sapiens 211-216 33990641-6 2021 Upon CDDP treatment, EA predominantly enhanced ROS generation, ASK1-p38/c-Jun N-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) pathway activation, and ultimately cell death, all of which were suppressed either by co-treatment of the NADPH oxidase (Nox) inhibitor Apocynin, or by knocking out its regulatory protein, receptor-interacting protein 1 (RIP1). Cisplatin 5-9 mitogen-activated protein kinase 8 Homo sapiens 97-100 33921192-6 2021 Western blot assay demonstrated that resveratrol combined with cisplatin significantly reduced the expression of fibronectin, vimentin, P-AKT, P-PI3K, P-JNK, P-ERK, Sma2, and Smad3 induced by TGF-beta1 (p < 0.05), and increased the expression of E-cadherin (p < 0.05), respectively. Cisplatin 63-72 mitogen-activated protein kinase 8 Homo sapiens 153-156 33959604-9 2021 In addition, the activation of ER stress and the JNK signaling pathway prompted by IATL and cisplatin was also reversed by NAC pretreatment. Cisplatin 92-101 mitogen-activated protein kinase 8 Homo sapiens 49-52 33456714-0 2021 Correction: Cepharanthine hydrochloride reverses the mdr1 (P-glycoprotein)-mediated esophageal squamous cell carcinoma cell cisplatin resistance through JNK and p53 signals. Cisplatin 124-133 mitogen-activated protein kinase 8 Homo sapiens 153-156 33460665-0 2021 RIPK1 contributes to cisplatin-induced apoptosis of esophageal squamous cell carcinoma cells via activation of JNK pathway. Cisplatin 21-30 mitogen-activated protein kinase 8 Homo sapiens 111-114 33072762-8 2020 Combination of ESI and cisplatin significantly increased the production of ROS, resulting in activation of the JNK signaling pathway in HCT116 and RKO cells. Cisplatin 23-32 mitogen-activated protein kinase 8 Homo sapiens 111-114 32781170-0 2020 Hydroxytyrosol enhances cisplatin-induced ototoxicity: Possible relation to the alteration in the activity of JNK and AIF pathways. Cisplatin 24-33 mitogen-activated protein kinase 8 Homo sapiens 110-113 32533982-5 2020 We also provided evidence that ZXF1 contributed to cisplatin resistance and cancer progression via activating ERK, JNK and p38-mediated MAPK signaling cascade. Cisplatin 51-60 mitogen-activated protein kinase 8 Homo sapiens 115-118 32695207-10 2020 Conclusion: Ginsenoside Rh1 alleviated HK-2 apoptosis in a cisplatin-induced injury model by inhibiting ROS production and the JNK/p53 pathway. Cisplatin 59-68 mitogen-activated protein kinase 8 Homo sapiens 127-130 32341033-10 2020 Mechanistically, PA facilitates JNK recruitment to c-JUN and its nuclear localization, leading to c-JUN activation upon cisplatin exposure. Cisplatin 120-129 mitogen-activated protein kinase 8 Homo sapiens 32-35 32884297-0 2020 MiR-140 Resensitizes Cisplatin-Resistant NSCLC Cells to Cisplatin Treatment Through the SIRT1/ROS/JNK Pathway. Cisplatin 21-30 mitogen-activated protein kinase 8 Homo sapiens 98-101 32884297-0 2020 MiR-140 Resensitizes Cisplatin-Resistant NSCLC Cells to Cisplatin Treatment Through the SIRT1/ROS/JNK Pathway. Cisplatin 56-65 mitogen-activated protein kinase 8 Homo sapiens 98-101 32884297-15 2020 Conclusion: MiR-140 resensitizes cisplatin-resistant NSCLC cells to cisplatin treatment through the SIRT1/ROS/JNK pathway. Cisplatin 33-42 mitogen-activated protein kinase 8 Homo sapiens 110-113 32884297-15 2020 Conclusion: MiR-140 resensitizes cisplatin-resistant NSCLC cells to cisplatin treatment through the SIRT1/ROS/JNK pathway. Cisplatin 68-77 mitogen-activated protein kinase 8 Homo sapiens 110-113 32277442-8 2020 Cisplatin treatment produced a similar response but it was associated with JNK activation rather than p38. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 75-78 31056532-9 2019 We then demonstrated that overexpression of miR-124 sensitized cisplatin-induced cytotoxicity against CD133+ hepatocellular carcinoma cells by targeting SIRT1/ROS/JNK pathway. Cisplatin 63-72 mitogen-activated protein kinase 8 Homo sapiens 163-166 32308804-7 2020 In addition, the combination treatment of PLB and cisplatin resulted in a synergistic inhibition of TSCC viability, apoptosis, and autophagy by increasing intracellular ROS, which may be achieved by activating JNK and inhibiting AKT/mTOR signaling pathways. Cisplatin 50-59 mitogen-activated protein kinase 8 Homo sapiens 210-213 32238696-6 2020 Moreover, cisplatin-induced JNK activation was attenuated in TRAF2-deficient cells, and pharmacological inhibition of JNK signaling suppressed p53 stabilization. Cisplatin 10-19 mitogen-activated protein kinase 8 Homo sapiens 28-31 32238696-6 2020 Moreover, cisplatin-induced JNK activation was attenuated in TRAF2-deficient cells, and pharmacological inhibition of JNK signaling suppressed p53 stabilization. Cisplatin 10-19 mitogen-activated protein kinase 8 Homo sapiens 118-121 31929796-10 2019 Cisplatin-responsive cell lines showed increased phosphorylation levels of JNK1/2/3 but decreased phosphorylation in cisplatin-resistant NCI-H2452 cells. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 75-83 31929796-14 2019 Based on our results, the induction of p38 or JNK1/3, or inhibition of AKT1 by, for example, BIA-6, might offer a positive synergistic effect by induction of an apoptotic response to cisplatin-based treatment, thus potentially enhancing the clinical outcome of MPM patients. Cisplatin 183-192 mitogen-activated protein kinase 8 Homo sapiens 46-52 31176737-8 2019 WZ26 combined with cisplatin markedly increases the accumulation of ROS, and thereby induces DNA damage and activation of JNK signaling pathway. Cisplatin 19-28 mitogen-activated protein kinase 8 Homo sapiens 122-125 31176737-10 2019 In addition, the activation of JNK signaling pathway prompted by WZ26 and cisplatin was also reversed by NAC pretreatment. Cisplatin 74-83 mitogen-activated protein kinase 8 Homo sapiens 31-34 31056532-0 2019 MiR-124 sensitizes cisplatin-induced cytotoxicity against CD133+ hepatocellular carcinoma cells by targeting SIRT1/ROS/JNK pathway. Cisplatin 19-28 mitogen-activated protein kinase 8 Homo sapiens 119-122 30868675-9 2019 Further study showed that CAF-CM enhanced cisplatin resistance by inhibiting cisplatin-induced apoptosis, determined by repression of caspase-3 and caspase-8, through activation of the ANXA3/JNK pathway. Cisplatin 42-51 mitogen-activated protein kinase 8 Homo sapiens 191-194 30868675-9 2019 Further study showed that CAF-CM enhanced cisplatin resistance by inhibiting cisplatin-induced apoptosis, determined by repression of caspase-3 and caspase-8, through activation of the ANXA3/JNK pathway. Cisplatin 77-86 mitogen-activated protein kinase 8 Homo sapiens 191-194 30868675-10 2019 Conversely, suppression of JNK activation by specific inhibitor retarded the effect of CAF-CM and ANXA3 on cisplatin sensitivity. Cisplatin 107-116 mitogen-activated protein kinase 8 Homo sapiens 27-30 29458150-9 2018 Moreover, treatment with 30 muM cisplatin elicited the formation of ROS, which, in turn, led to PINK1 activation, parkin recruitment, autophagy formation and JNK pathway relevant to apoptosis in HEI-OC1 cells, HCs, and SGNs. Cisplatin 32-41 mitogen-activated protein kinase 8 Homo sapiens 158-161 30032449-13 2018 Therapeutically, enhancement of GRIM19 expression or employment of p38/JNK inhibitors may serve as resensitizing therapies for subgroups of CDDP-resistant or refractory BC patients. Cisplatin 140-144 mitogen-activated protein kinase 8 Homo sapiens 71-74 30614075-8 2019 In addition, the core fucosylation could regulate the phosphorylation of cDDP-resistance-associated molecules, such as AKT, ERK, JNK, and mTOR. Cisplatin 73-77 mitogen-activated protein kinase 8 Homo sapiens 129-132 30922965-13 2019 INTERPRETATION: PDIA6 is overexpressed in NSCLC and inhibits cisplatin-induced NSCLC cell apoptosis and autophagy via the MAP4K1/JNK/c-Jun signaling pathway, suggesting that PDIA6 may serve as a biomarker and therapeutic target for NSCLC patients. Cisplatin 61-70 mitogen-activated protein kinase 8 Homo sapiens 129-132 29103194-12 2018 CONCLUSIONS: Astragalus polysaccharides increased the sensitivity of SKOV3 cells to cisplatin potentially by activating the JNK pathway. Cisplatin 84-93 mitogen-activated protein kinase 8 Homo sapiens 124-127 29512740-8 2018 Taken together, the findings of the present study indicate that PDCD4 enhances the sensitivity of BCa cells to cisplatin, partially via regulation of the JNK/c-Jun pathway, and reverses EMT. Cisplatin 111-120 mitogen-activated protein kinase 8 Homo sapiens 154-157 29432736-0 2018 miR-223/Hsp70/JNK/JUN/miR-223 feedback loop modulates the chemoresistance of osteosarcoma to cisplatin. Cisplatin 93-102 mitogen-activated protein kinase 8 Homo sapiens 14-17 29432736-8 2018 In summary, miR-223, Hsp70 and downstream JNK/JUN formed a feedback loop to modulate the chemoresistance of OS to CDDP. Cisplatin 114-118 mitogen-activated protein kinase 8 Homo sapiens 42-45 29512740-0 2018 Programmed cell death 4 overexpression enhances sensitivity to cisplatin via the JNK/c-Jun signaling pathway in bladder cancer. Cisplatin 63-72 mitogen-activated protein kinase 8 Homo sapiens 81-84 29393335-5 2018 Additionally, the mechanism underlying the cis-DDP-induced apoptosis was indicated to involve the activation of p53, c-Jun-N-terminal kinase (JNK) and p38 signaling. Cisplatin 43-50 mitogen-activated protein kinase 8 Homo sapiens 117-140 29393335-5 2018 Additionally, the mechanism underlying the cis-DDP-induced apoptosis was indicated to involve the activation of p53, c-Jun-N-terminal kinase (JNK) and p38 signaling. Cisplatin 43-50 mitogen-activated protein kinase 8 Homo sapiens 142-145 29071589-0 2018 Melatonin increases human cervical cancer HeLa cells apoptosis induced by cisplatin via inhibition of JNK/Parkin/mitophagy axis. Cisplatin 74-83 mitogen-activated protein kinase 8 Homo sapiens 102-105 29940575-13 2018 Phosphorylation of JNK and the subsequent mitochondrial apoptosis were triggered by the combination of cisplatin and anti-miR-20a. Cisplatin 103-112 mitogen-activated protein kinase 8 Homo sapiens 19-22 29940575-14 2018 CONCLUSIONS: Knockdown of miR-20a enhanced sensitivity of colorectal cancer cells to cisplatin through the ROS/ASK1/JNK pathway. Cisplatin 85-94 mitogen-activated protein kinase 8 Homo sapiens 116-119 28597042-7 2017 Preincubation with JNK-specific inhibitor, SP600125, significantly inhibited these genes" expression at mRNA and protein levels, enhanced chemosensitivity of lung cancer cells to cisplatin, and promoted cisplatin-induced apoptosis. Cisplatin 179-188 mitogen-activated protein kinase 8 Homo sapiens 19-22 29039558-0 2017 Insulin in combination with cisplatin induces the apoptosis of ovarian cancer cells via p53 and JNK activation. Cisplatin 28-37 mitogen-activated protein kinase 8 Homo sapiens 96-99 28650468-9 2017 Thus, this work indicates that suppression of JNK1/2 activity by MKP-1 maintains PARP-1 levels and suggests that MKP-1-mediated cisplatin resistance can be bypassed by PARP-1 inhibition. Cisplatin 128-137 mitogen-activated protein kinase 8 Homo sapiens 46-52 28886730-0 2017 Annexin A2 contributes to cisplatin resistance by activation of JNK-p53 pathway in non-small cell lung cancer cells. Cisplatin 26-35 mitogen-activated protein kinase 8 Homo sapiens 64-67 28886730-11 2017 CONCLUSIONS: These data suggested that Annexin A2 induces cisplatin resistance of NSCLCs via regulation of JNK/c-Jun/p53 signaling, and provided an evidence that blockade of Annexin A2 could serve as a novel therapeutic approach for overcoming drug resistance in NSCLCs. Cisplatin 58-67 mitogen-activated protein kinase 8 Homo sapiens 107-110 29033791-0 2017 Protein Synthesis Inhibition and Activation of the c-Jun N-Terminal Kinase Are Potential Contributors to Cisplatin Ototoxicity. Cisplatin 105-114 mitogen-activated protein kinase 8 Homo sapiens 51-74 29033791-8 2017 Similar to what was found after gentamicin exposure, cisplatin activates both the c-Jun N-terminal kinase (JNK) and mammalian target of rapamycin (mTOR) pathways. Cisplatin 53-62 mitogen-activated protein kinase 8 Homo sapiens 82-105 29033791-8 2017 Similar to what was found after gentamicin exposure, cisplatin activates both the c-Jun N-terminal kinase (JNK) and mammalian target of rapamycin (mTOR) pathways. Cisplatin 53-62 mitogen-activated protein kinase 8 Homo sapiens 107-110 28597042-7 2017 Preincubation with JNK-specific inhibitor, SP600125, significantly inhibited these genes" expression at mRNA and protein levels, enhanced chemosensitivity of lung cancer cells to cisplatin, and promoted cisplatin-induced apoptosis. Cisplatin 203-212 mitogen-activated protein kinase 8 Homo sapiens 19-22 28597042-8 2017 CONCLUSION: Our data suggest that the JNK signaling pathway plays an important role in cisplatin resistance. Cisplatin 87-96 mitogen-activated protein kinase 8 Homo sapiens 38-41 27751820-0 2016 Inhibition of JNK and prothymosin-alpha sensitizes hepatocellular carcinoma cells to cisplatin. Cisplatin 85-94 mitogen-activated protein kinase 8 Homo sapiens 14-17 28598976-10 2017 Maximal sensitivity to cisplatin was obtained with simultaneous inhibition of both autophagy and JNK pathway. Cisplatin 23-32 mitogen-activated protein kinase 8 Homo sapiens 97-100 28287190-0 2017 NLRX1 accelerates cisplatin-induced ototoxity in HEI-OC1 cells via promoting generation of ROS and activation of JNK signaling pathway. Cisplatin 18-27 mitogen-activated protein kinase 8 Homo sapiens 113-116 28287190-8 2017 The findings from this work reveal that NLRX1 sensitizes HEI-OC1 cells to cisplatin-induced apoptosis via activation of ROS/JNK signaling pathway, suggesting that NLRX1 acts as an important regulator of the cisplatin-elicited ototoxity. Cisplatin 74-83 mitogen-activated protein kinase 8 Homo sapiens 124-127 28287190-8 2017 The findings from this work reveal that NLRX1 sensitizes HEI-OC1 cells to cisplatin-induced apoptosis via activation of ROS/JNK signaling pathway, suggesting that NLRX1 acts as an important regulator of the cisplatin-elicited ototoxity. Cisplatin 207-216 mitogen-activated protein kinase 8 Homo sapiens 124-127 28232663-11 2017 In conclusion, the Epac-Rap1-Akt pathway mediates cAMP signaling-induced inhibition of JNK-dependent HDAC8 degradation, and the resulting HDAC8 increase augments cisplatin-induced apoptosis by repressing TIPRL expression in H1299 lung cancer cells. Cisplatin 162-171 mitogen-activated protein kinase 8 Homo sapiens 87-90 27751820-5 2016 Cisplatin inhibits both the JNK pathway and PTMA in a dose-dependent manner. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 28-31 27751820-6 2016 Treatment with a JNK inhibitor also reduces PTMA protein stability and sensitizes HCC cells to cisplatin. Cisplatin 95-104 mitogen-activated protein kinase 8 Homo sapiens 17-20 27751820-10 2016 Our results indicate that PTMA is positively regulated by JNK and protects HCC cells against cisplatin-induced cell death. Cisplatin 93-102 mitogen-activated protein kinase 8 Homo sapiens 58-61 28101169-9 2016 In conclusion, abnormal activation of Wnt/beta-catenin and Wnt/JNK signaling pathways in ovarian cancer cells promotes cisplatin resistance, while the Wnt/Ca2+ signaling pathway reduces cisplatin resistance. Cisplatin 119-128 mitogen-activated protein kinase 8 Homo sapiens 63-66 27825085-0 2016 AKT2 inhibition of cisplatin-induced JNK/p38 and Bax activation by phosphorylation of ASK1. Cisplatin 19-28 mitogen-activated protein kinase 8 Homo sapiens 37-40 27374471-7 2016 Recent studies suggest that JNK signalling pathway plays a major role in deciding the fate of the cell and inducing resistance to cDDP-induced apoptosis in human tumours. Cisplatin 130-134 mitogen-activated protein kinase 8 Homo sapiens 28-31 27374471-9 2016 Therefore, it is suggested that JNK signal pathway is a double-edged sword in cDDP treatment, simultaneously being a significant pro-apoptosis factor but also being associated with increased resistance to cisplatin-based chemotherapy. Cisplatin 78-82 mitogen-activated protein kinase 8 Homo sapiens 32-35 27374471-9 2016 Therefore, it is suggested that JNK signal pathway is a double-edged sword in cDDP treatment, simultaneously being a significant pro-apoptosis factor but also being associated with increased resistance to cisplatin-based chemotherapy. Cisplatin 205-214 mitogen-activated protein kinase 8 Homo sapiens 32-35 27374471-10 2016 This review focuses on current knowledge concerning the role of JNK in cell response to cDDP, as well as their role in cisplatin resistance. Cisplatin 88-92 mitogen-activated protein kinase 8 Homo sapiens 64-67 27779694-8 2016 In conclusion, fentanyl reduces the sensitivity of cisplatin in lung cancer cells through the ROS-JNK-autophagy pathway, whereas the autophagy inhibitor 3-MA may weaken this effect. Cisplatin 51-60 mitogen-activated protein kinase 8 Homo sapiens 98-101 27193727-0 2016 Fenofibrate reduces cisplatin-induced apoptosis of renal proximal tubular cells via inhibition of JNK and p38 pathways. Cisplatin 20-29 mitogen-activated protein kinase 8 Homo sapiens 98-101 27659012-5 2016 Cisplatin-induced JNK activation was a key regulator of this ATF3 induction. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 18-21 27659012-6 2016 Interestingly, in both resistant sublines, this JNK induction was abrogated, and the expression of an activated JNK construct in these cells enhanced both cisplatin-induced cytotoxicity and ATF3 induction. Cisplatin 155-164 mitogen-activated protein kinase 8 Homo sapiens 112-115 27313779-11 2016 Knockdown of p53 decreased cisplatin"s induction of c-Jun N-terminal kinase 1/2 (JNK1/2) activation, whereas inhibition of JNK1/2 activation increased chemosensitivity. Cisplatin 27-36 mitogen-activated protein kinase 8 Homo sapiens 52-79 27313779-11 2016 Knockdown of p53 decreased cisplatin"s induction of c-Jun N-terminal kinase 1/2 (JNK1/2) activation, whereas inhibition of JNK1/2 activation increased chemosensitivity. Cisplatin 27-36 mitogen-activated protein kinase 8 Homo sapiens 81-87 27313779-11 2016 Knockdown of p53 decreased cisplatin"s induction of c-Jun N-terminal kinase 1/2 (JNK1/2) activation, whereas inhibition of JNK1/2 activation increased chemosensitivity. Cisplatin 27-36 mitogen-activated protein kinase 8 Homo sapiens 81-85 27193727-7 2016 Treating cells with cisplatin induced reactive oxygen species (ROS), c-JUN N-terminal kinase (JNK), and p38 kinase (p38), but not extracellular signal-regulated kinase (ERK). Cisplatin 20-29 mitogen-activated protein kinase 8 Homo sapiens 69-92 27193727-7 2016 Treating cells with cisplatin induced reactive oxygen species (ROS), c-JUN N-terminal kinase (JNK), and p38 kinase (p38), but not extracellular signal-regulated kinase (ERK). Cisplatin 20-29 mitogen-activated protein kinase 8 Homo sapiens 94-97 27193727-8 2016 Fenofibrate reversed cisplatin-induced JNK and p38 activation, but had no effect on ROS production. Cisplatin 21-30 mitogen-activated protein kinase 8 Homo sapiens 39-42 27193727-9 2016 The findings suggest fenofibrate"s protective effect on cisplatin-induced cytotoxicity is mediated by inhibition of JNK and p38. Cisplatin 56-65 mitogen-activated protein kinase 8 Homo sapiens 116-119 26534836-0 2016 Time-staggered inhibition of JNK effectively sensitizes chemoresistant ovarian cancer cells to cisplatin and paclitaxel. Cisplatin 95-104 mitogen-activated protein kinase 8 Homo sapiens 29-32 26534836-3 2016 In the present study, while investigating the mechanism underlying the chemoresistance of ovarian cancer, we found that JNK may have a key role in the resistance of ovarian cancer cells to cisplatin and paclitaxel. Cisplatin 189-198 mitogen-activated protein kinase 8 Homo sapiens 120-123 26534836-4 2016 Importantly, whereas simultaneous application of a JNK inhibitor and either of the chemotherapeutic agents had contrasting effects for cisplatin (enhanced cytotoxicity) and paclitaxel (decreased cytotoxicity), JNK inhibitor treatment prior to chemotherapeutic agent application invariably enhanced the cytotoxicity of both drugs, suggesting that the basal JNK activity is commonly involved in the chemoresistance of ovarian cancer cells to cisplatin and paclitaxel in contrast to drug-induced JNK activity which may have different roles for these two drugs. Cisplatin 135-144 mitogen-activated protein kinase 8 Homo sapiens 51-54 26534836-4 2016 Importantly, whereas simultaneous application of a JNK inhibitor and either of the chemotherapeutic agents had contrasting effects for cisplatin (enhanced cytotoxicity) and paclitaxel (decreased cytotoxicity), JNK inhibitor treatment prior to chemotherapeutic agent application invariably enhanced the cytotoxicity of both drugs, suggesting that the basal JNK activity is commonly involved in the chemoresistance of ovarian cancer cells to cisplatin and paclitaxel in contrast to drug-induced JNK activity which may have different roles for these two drugs. Cisplatin 440-449 mitogen-activated protein kinase 8 Homo sapiens 51-54 26592553-0 2015 MLN4924 Synergistically Enhances Cisplatin-induced Cytotoxicity via JNK and Bcl-xL Pathways in Human Urothelial Carcinoma. Cisplatin 33-42 mitogen-activated protein kinase 8 Homo sapiens 68-71 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 mitogen-activated protein kinase 8 Homo sapiens 0-23 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 mitogen-activated protein kinase 8 Homo sapiens 25-28 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 mitogen-activated protein kinase 8 Homo sapiens 111-114 26049416-14 2015 We also demonstrated that cisplatin in combination with PP2 or SP600125 could be clinically beneficial, as inhibition of Src or JNK in an APC-mutant breast cancer patient may alleviate the resistance induced by mutant APC. Cisplatin 26-35 mitogen-activated protein kinase 8 Homo sapiens 128-131 26118633-7 2015 More importantly, SSD effectively blocked the DDP-induced activation of NF-kappaB, P38, JNK, and MAPKs. Cisplatin 46-49 mitogen-activated protein kinase 8 Homo sapiens 88-91 25563368-0 2015 FOXM1 overexpression is associated with cisplatin resistance in non-small cell lung cancer and mediates sensitivity to cisplatin in A549 cells via the JNK/mitochondrial pathway. Cisplatin 119-128 mitogen-activated protein kinase 8 Homo sapiens 151-154 25793618-8 2015 In particular, cisplatin treatment led to decreased ERK-, JNK- and c-Jun phosphorylation in alpha-catulin knockdown melanoma cells, which was accompanied by enhanced apoptosis compared to control cells. Cisplatin 15-24 mitogen-activated protein kinase 8 Homo sapiens 58-62 25682199-6 2015 While cisplatin slightly potentiated the JNK/Bcl2/Beclin1 pathway for autophagy activation, its combination with Chal-24 strongly triggered proteasomal degradation of the cellular inhibitor of apoptosis proteins (c-IAPs) and formation of the Ripoptosome complex that contains RIP1, FADD and caspase 8. Cisplatin 6-15 mitogen-activated protein kinase 8 Homo sapiens 41-44 25563368-8 2015 Moreover, we showed that the downregulation of FoxM1 enhanced cisplatin-induced A549/CDDP cell apoptosis through the activation of the c-Jun NH2-terminal kinase (JNK)/mitochondrial pathway. Cisplatin 62-71 mitogen-activated protein kinase 8 Homo sapiens 135-160 25563368-8 2015 Moreover, we showed that the downregulation of FoxM1 enhanced cisplatin-induced A549/CDDP cell apoptosis through the activation of the c-Jun NH2-terminal kinase (JNK)/mitochondrial pathway. Cisplatin 62-71 mitogen-activated protein kinase 8 Homo sapiens 162-165 24675421-0 2014 Retaining MKP1 expression and attenuating JNK-mediated apoptosis by RIP1 for cisplatin resistance through miR-940 inhibition. Cisplatin 77-86 mitogen-activated protein kinase 8 Homo sapiens 42-45 25351964-4 2015 Addition of either small interfering JNK1-siRNA or JNK2-siRNA induced decreased DNA repair and sensitized the T98G glioblastoma cells to the DNA damaging drug cisplatin (cis-diamminedichloroplatinum). Cisplatin 159-168 mitogen-activated protein kinase 8 Homo sapiens 37-41 25152024-0 2014 Mig-2 attenuates cisplatin-induced apoptosis of human glioma cells in vitro through AKT/JNK and AKT/p38 signaling pathways. Cisplatin 17-26 mitogen-activated protein kinase 8 Homo sapiens 88-91 25006835-5 2014 Cisplatin induced hyperphosphorylation of p38alpha MAPK and AMPKalpha1, whereas oxoplatin treatment resulted in increased phosphorylation of a large number of signaling proteins involved in stress response/drug resistance, including JNK, GSK-3alpha, AMPKalpha1, src kinases, STATs, CHK-2 and especially focal adhesion kinase (FAK). Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 233-236 24686174-6 2014 Moreover, basal and cisplatin-induced activity of the stress response kinase JNK is enhanced in HOIP-depleted cells and, conversely, JNK inhibition can increase cellular resistance to cisplatin and reverse the apoptotic hyperactivation in HOIP-depleted cells. Cisplatin 20-29 mitogen-activated protein kinase 8 Homo sapiens 77-80 24686174-6 2014 Moreover, basal and cisplatin-induced activity of the stress response kinase JNK is enhanced in HOIP-depleted cells and, conversely, JNK inhibition can increase cellular resistance to cisplatin and reverse the apoptotic hyperactivation in HOIP-depleted cells. Cisplatin 20-29 mitogen-activated protein kinase 8 Homo sapiens 133-136 24686174-6 2014 Moreover, basal and cisplatin-induced activity of the stress response kinase JNK is enhanced in HOIP-depleted cells and, conversely, JNK inhibition can increase cellular resistance to cisplatin and reverse the apoptotic hyperactivation in HOIP-depleted cells. Cisplatin 184-193 mitogen-activated protein kinase 8 Homo sapiens 77-80 24686174-6 2014 Moreover, basal and cisplatin-induced activity of the stress response kinase JNK is enhanced in HOIP-depleted cells and, conversely, JNK inhibition can increase cellular resistance to cisplatin and reverse the apoptotic hyperactivation in HOIP-depleted cells. Cisplatin 184-193 mitogen-activated protein kinase 8 Homo sapiens 133-136 23584473-8 2014 Hence, our study revealed a novel mechanism, by which PKA/Smurf1 antagonizes the downregulating effect of JNK on Nur77, leading to the accumulation of Nur77 for apoptosis induction triggered by cisplatin. Cisplatin 194-203 mitogen-activated protein kinase 8 Homo sapiens 106-109 25152024-11 2014 CONCLUSION: Mig-2 significantly attenuates the antitumor action of cisplatin against human glioma cells in vitro through AKT/JNK and AKT/p38 signaling pathways. Cisplatin 67-76 mitogen-activated protein kinase 8 Homo sapiens 125-128 23543357-5 2014 In cellular mechanism study, co-treatment of cordycepin and cisplatin induced more stress-activated protein kinase/Jun terminal kinase (JNK), the expressions of caspase-7, and the cleavage of poly ADP-ribose polymerase (PARP) as compared to cisplatin or cordycepin alone treatment (P <0.05). Cisplatin 60-69 mitogen-activated protein kinase 8 Homo sapiens 136-139 23543357-6 2014 CONCLUSION: Cisplatin and cordycepin possess synergistically apoptotic effect through the activation of JNK/caspase-7/PARP pathway in human OC3 oral cancer cell line. Cisplatin 12-21 mitogen-activated protein kinase 8 Homo sapiens 104-107 25028967-7 2014 Over-expression of RASSF6 in highly metastatic NPC cells could enhance the phosphorylation of JNK when exposed to cisplatin or radiation treatment, while knocking down RASSF6 in low metastatic NPC cells could reduce the level of phospho-JNK when exposed to the same treatments. Cisplatin 114-123 mitogen-activated protein kinase 8 Homo sapiens 94-97 24865582-0 2014 Upregulation of miR-21 in cisplatin resistant ovarian cancer via JNK-1/c-Jun pathway. Cisplatin 26-35 mitogen-activated protein kinase 8 Homo sapiens 65-70 24865582-13 2014 These results suggest that the JNK-1/c-Jun/miR-21 pathway contributes to the cisplatin resistance of ovarian cancer cells and demonstrated that miR-21 is a plausible target to overcome cisplatin resistance. Cisplatin 77-86 mitogen-activated protein kinase 8 Homo sapiens 31-36 24865582-13 2014 These results suggest that the JNK-1/c-Jun/miR-21 pathway contributes to the cisplatin resistance of ovarian cancer cells and demonstrated that miR-21 is a plausible target to overcome cisplatin resistance. Cisplatin 185-194 mitogen-activated protein kinase 8 Homo sapiens 31-36 24675421-3 2014 In lung cancer cells, knockdown of RIP1 substantially increased cisplatin-induced apoptotic cytotoxicity, which was associated with robust JNK activation. Cisplatin 64-73 mitogen-activated protein kinase 8 Homo sapiens 139-142 24675421-7 2014 Knockdown of miR-940 restored MKP1 expression and attenuated cisplatin-induced JNK activation and cytotoxicity. Cisplatin 61-70 mitogen-activated protein kinase 8 Homo sapiens 79-82 24675421-8 2014 Importantly, ectopic expression of MKP1 effectively attenuated cisplatin-induced JNK activation and cytotoxicity. Cisplatin 63-72 mitogen-activated protein kinase 8 Homo sapiens 81-84 24675421-10 2014 Altogether, our results suggest that RIP1 contributes to cisplatin resistance by suppressing JNK activation that involves releasing miR-940-mediated inhibition of MKP1 and suppressing activation of MKK4. Cisplatin 57-66 mitogen-activated protein kinase 8 Homo sapiens 93-96 24055030-5 2013 Pharmacological inhibition of JNK or knockdown of JNK significantly reduces the ability of MUC1 to inhibit cisplatin-induced apoptosis. Cisplatin 107-116 mitogen-activated protein kinase 8 Homo sapiens 30-33 24115572-0 2013 Inhibition of p38 MAPK sensitizes tumour cells to cisplatin-induced apoptosis mediated by reactive oxygen species and JNK. Cisplatin 50-59 mitogen-activated protein kinase 8 Homo sapiens 118-121 24115572-4 2013 We show that p38 MAPK inhibition results in ROS upregulation, which in turn activates the JNK pathway via inactivation of phosphatases, sensitizing human tumour cells to cisplatin-induced apoptosis. Cisplatin 170-179 mitogen-activated protein kinase 8 Homo sapiens 90-93 23929259-4 2013 This liable action of cisplatin on kidneys is mediated by altered intracellular signalling pathways such as mitogen-activated protein kinase (MAPK), extracellular regulated kinase (ERK), or C- Jun N terminal kinase/stress-activated protein kinase (JNK/SAPK). Cisplatin 22-31 mitogen-activated protein kinase 8 Homo sapiens 248-256 24055030-5 2013 Pharmacological inhibition of JNK or knockdown of JNK significantly reduces the ability of MUC1 to inhibit cisplatin-induced apoptosis. Cisplatin 107-116 mitogen-activated protein kinase 8 Homo sapiens 50-53 23900581-7 2013 We showed that cisplatin treatment increased JNK-1 and JNK-2 activity and expression in both LNCaP and PC-3 cells. Cisplatin 15-24 mitogen-activated protein kinase 8 Homo sapiens 45-50 23900581-9 2013 Our observations indicate that JNK-1 and JNK-2 may be involved in the chemoresistance observed in prostate cancer cells treated with cisplatin and that blocking the stimulation of Jun kinase (JNK) signaling may be important for regulating the susceptibility to cisplatin of prostate cancer. Cisplatin 133-142 mitogen-activated protein kinase 8 Homo sapiens 31-36 23900581-9 2013 Our observations indicate that JNK-1 and JNK-2 may be involved in the chemoresistance observed in prostate cancer cells treated with cisplatin and that blocking the stimulation of Jun kinase (JNK) signaling may be important for regulating the susceptibility to cisplatin of prostate cancer. Cisplatin 261-270 mitogen-activated protein kinase 8 Homo sapiens 31-36 23817665-9 2013 Furthermore, beta-elemene blocked the cisplatin-stimulated increase in the level of phosphorylated c-Jun NH2-terminal kinase (JNK) in these cells. Cisplatin 38-47 mitogen-activated protein kinase 8 Homo sapiens 99-124 23817665-9 2013 Furthermore, beta-elemene blocked the cisplatin-stimulated increase in the level of phosphorylated c-Jun NH2-terminal kinase (JNK) in these cells. Cisplatin 38-47 mitogen-activated protein kinase 8 Homo sapiens 126-129 21324906-2 2011 Here we show that the SEK1/MKK4-mediated dual phosphorylation of SAPK/JNK (Thr-183/Tyr-185) correlates with the level of cisplatin-DNA adducts at late times (16-24 h) after drug treatment in both human and mouse cells. Cisplatin 121-130 mitogen-activated protein kinase 8 Homo sapiens 70-73 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 mitogen-activated protein kinase 8 Homo sapiens 161-164 22900074-0 2012 TAp73-mediated the activation of c-Jun N-terminal kinase enhances cellular chemosensitivity to cisplatin in ovarian cancer cells. Cisplatin 95-104 mitogen-activated protein kinase 8 Homo sapiens 33-56 22900074-5 2012 Inhibition of JNK activity by a specific inhibitor or small interfering RNA (siRNA) significantly abrogated TAp73-mediated apoptosis induced by cisplatin. Cisplatin 144-153 mitogen-activated protein kinase 8 Homo sapiens 14-17 22900074-7 2012 Our study has demonstrated that TAp73 activated the JNK apoptotic signaling pathway in response to cisplatin in ovarian cancer cells. Cisplatin 99-108 mitogen-activated protein kinase 8 Homo sapiens 52-55 23720056-9 2013 Mechanistic studies showed that the cisplatin-induced cytoplasmic TR3 translocation required for apoptosis induction was regulated by JNK activation and inhibition of Akt. Cisplatin 36-45 mitogen-activated protein kinase 8 Homo sapiens 134-137 23720056-10 2013 Finally, cisplatin resistance was partially overcome by ectopic TR3 overexpression and by treatment with the JNK activator anisomycin and Akt pathway inhibitor, wortmannin. Cisplatin 9-18 mitogen-activated protein kinase 8 Homo sapiens 109-112 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 mitogen-activated protein kinase 8 Homo sapiens 40-43 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 mitogen-activated protein kinase 8 Homo sapiens 107-110 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 mitogen-activated protein kinase 8 Homo sapiens 81-84 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 mitogen-activated protein kinase 8 Homo sapiens 170-173 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 mitogen-activated protein kinase 8 Homo sapiens 190-193 22142405-9 2012 All three main Mitogen-activated protein kinases (MAPK) families - extracellular signal-regulated kinases (ERK), c-Jun-N-terminal kinase (JNK) and p38 were activated after treatment of DPSCs with cisplatin. Cisplatin 196-205 mitogen-activated protein kinase 8 Homo sapiens 113-136 22142405-9 2012 All three main Mitogen-activated protein kinases (MAPK) families - extracellular signal-regulated kinases (ERK), c-Jun-N-terminal kinase (JNK) and p38 were activated after treatment of DPSCs with cisplatin. Cisplatin 196-205 mitogen-activated protein kinase 8 Homo sapiens 138-141 21684138-5 2012 Cisplatin triggered marked activation of stress signaling pathways [p53, Jun N-terminal kinase (JNK), and p38-alpha mitogen-activated protein kinase (MAPK)] and promoted cell death in the kidneys (increased DNA fragmentation, caspases-3/7 activity, terminal deoxynucleotidyl transferase-mediated uridine triphosphate nick-end labeling), associated with attenuation of various prosurvival signaling pathways [e.g., extracellular signal-regulated kinase (ERK) and p38-beta MAPK]. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 73-94 21684138-5 2012 Cisplatin triggered marked activation of stress signaling pathways [p53, Jun N-terminal kinase (JNK), and p38-alpha mitogen-activated protein kinase (MAPK)] and promoted cell death in the kidneys (increased DNA fragmentation, caspases-3/7 activity, terminal deoxynucleotidyl transferase-mediated uridine triphosphate nick-end labeling), associated with attenuation of various prosurvival signaling pathways [e.g., extracellular signal-regulated kinase (ERK) and p38-beta MAPK]. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 96-99 21684138-8 2012 Thus, the cisplatin-induced nephropathy is associated with activation of various cell death and proinflammatory pathways (p53, JNK, p38-alpha, TNF-alpha and NF-kappaB) and impairments of key prosurvival signaling mechanisms (ERK and p38-beta). Cisplatin 10-19 mitogen-activated protein kinase 8 Homo sapiens 127-130 21324906-4 2011 A defect in transcription-coupled nucleotide excision repair resting on a mutation in Cockayne syndrome group B protein promoted the late SAPK/JNK activation following cisplatin exposure. Cisplatin 168-177 mitogen-activated protein kinase 8 Homo sapiens 143-146 21324906-7 2011 Late activation of SAPK/JNK stimulated by cisplatin-induced DNA lesions was reduced in the absence of specific DNA repair proteins, such as xeroderma pigmentosum protein C, pointing to an essential function of individual repair factors in DNA damage signaling to SAPK/JNK. Cisplatin 42-51 mitogen-activated protein kinase 8 Homo sapiens 24-27 21324906-7 2011 Late activation of SAPK/JNK stimulated by cisplatin-induced DNA lesions was reduced in the absence of specific DNA repair proteins, such as xeroderma pigmentosum protein C, pointing to an essential function of individual repair factors in DNA damage signaling to SAPK/JNK. Cisplatin 42-51 mitogen-activated protein kinase 8 Homo sapiens 268-271 21324906-8 2011 Collectively, the data indicate that late SAPK/JNK activation is triggered by non-repaired cisplatin adducts in transcribed genes and involves replication-associated events, DSBs, tyrosine kinases, Rho GTPases, and specific repair factors. Cisplatin 91-100 mitogen-activated protein kinase 8 Homo sapiens 47-50 19787270-4 2009 TBB and DMAT treatment together with cisplatin lead to an inhibition of cisplatin-induced stress signaling (as detected by phosphorylation of JNK and H2AX). Cisplatin 37-46 mitogen-activated protein kinase 8 Homo sapiens 142-145 20106899-8 2010 Conversely, in transfected cells, the strong activation of Jun N-terminal kinase (JNK)-1 induced by cisplatin at later times (10-20 h) was completely prevented. Cisplatin 100-109 mitogen-activated protein kinase 8 Homo sapiens 59-88 21857081-10 2011 These results demonstrate that the expression of HO-1 induced by phloretin is mediated by both the JNK pathway and Nrf2; the expression inhibits cisplatin-induced apoptosis in HEI-OC1 cells. Cisplatin 145-154 mitogen-activated protein kinase 8 Homo sapiens 99-102 19910452-9 2010 MDA-7/IL-24 and cisplatin interacted in a greater than additive fashion to kill tumor cells that was dependent on a further elevation of JNK1/2 activity and recruitment of the extrinsic CD95 pathway. Cisplatin 16-25 mitogen-activated protein kinase 8 Homo sapiens 137-143 19787270-4 2009 TBB and DMAT treatment together with cisplatin lead to an inhibition of cisplatin-induced stress signaling (as detected by phosphorylation of JNK and H2AX). Cisplatin 72-81 mitogen-activated protein kinase 8 Homo sapiens 142-145 19723115-8 2009 Cisplatin alone and its combination with AG1478 increased the phosphorylation of p38 and c-Jun N-terminal kinase (JNK) in both cell lines. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 89-112 19723115-8 2009 Cisplatin alone and its combination with AG1478 increased the phosphorylation of p38 and c-Jun N-terminal kinase (JNK) in both cell lines. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 114-117 18391982-4 2008 As the mechanism, triptolide suppressed CDDP-induced p53 transcriptional activity, leading to p21 attenuation, which promoted apoptosis via the activation of c-Jun N-terminal kinase (JNK) and Bax. Cisplatin 40-44 mitogen-activated protein kinase 8 Homo sapiens 158-181 19471112-5 2009 In addition, cisplatin markedly reduced MMP2 activity in both conditioned media and cell lysates, increased p38 MAPK and JNK phosphorylation, but did not affect ERK phosphorylation. Cisplatin 13-22 mitogen-activated protein kinase 8 Homo sapiens 121-124 19471112-8 2009 CONCLUSION: These results suggested that cisplatin induced a reduction of endothelial cell migration through an inhibition of MMP2 activity by downstream signal transduction pathways independent of JNK and p38 MAPK activation. Cisplatin 41-50 mitogen-activated protein kinase 8 Homo sapiens 198-201 19258036-10 2009 Finally, our proteomic analysis revealed that cisplatin-stimulated plaa(high) cells contained higher levels of phosphorylated JNK/c-Jun and FasL than did plaa(low) cells treated the same way. Cisplatin 46-55 mitogen-activated protein kinase 8 Homo sapiens 126-129 19258036-11 2009 In summary, our data indicated that PLAA induction enhanced cisplatin-induced-apoptosis through four pathways, namely by: 1) accumulation of AA and mitochondrial damage, 2) downregulation of the cytoprotective clusterin, 3) upregulation of the pro-apoptotic IL-32, and 4) induction of JNK/c-Jun signaling and FasL expression. Cisplatin 60-69 mitogen-activated protein kinase 8 Homo sapiens 285-288 18726921-10 2008 Furthermore, delayed apoptosis induction following cisplatin treatment was observed in U2OS, in parallel to decreased JNK activation, increased MKP-1 expression and relatively increased cisplatin resistance. Cisplatin 51-60 mitogen-activated protein kinase 8 Homo sapiens 118-121 18372076-0 2008 Knockdown of Snail, a novel zinc finger transcription factor, via RNA interference increases A549 cell sensitivity to cisplatin via JNK/mitochondrial pathway. Cisplatin 118-127 mitogen-activated protein kinase 8 Homo sapiens 132-135 18372076-5 2008 The data showed that Snail depletion sensitized A549 cells to cisplatin possibly by inducing activation of JNK/mitochondrial pathway, suggesting critical roles of Snail in A549 cell chemoresistance to cisplatin and raising the possibility of Snail depletion as a promising approach to lung cancer therapy. Cisplatin 62-71 mitogen-activated protein kinase 8 Homo sapiens 107-110 18372076-5 2008 The data showed that Snail depletion sensitized A549 cells to cisplatin possibly by inducing activation of JNK/mitochondrial pathway, suggesting critical roles of Snail in A549 cell chemoresistance to cisplatin and raising the possibility of Snail depletion as a promising approach to lung cancer therapy. Cisplatin 201-210 mitogen-activated protein kinase 8 Homo sapiens 107-110 18391982-4 2008 As the mechanism, triptolide suppressed CDDP-induced p53 transcriptional activity, leading to p21 attenuation, which promoted apoptosis via the activation of c-Jun N-terminal kinase (JNK) and Bax. Cisplatin 40-44 mitogen-activated protein kinase 8 Homo sapiens 183-186 18331824-5 2008 The data showed that TWIST depletion significantly sensitized A549 cells to cisplatin by inducing activation of JNK/mitochondrial pathway but not ERK and p-38 pathways, suggesting critical roles of TWIST in A549 cell chemoresistance to cisplatin and raising the possibility of TWIST depletion as a promising approach to lung cancer therapy. Cisplatin 76-85 mitogen-activated protein kinase 8 Homo sapiens 112-115 18331824-5 2008 The data showed that TWIST depletion significantly sensitized A549 cells to cisplatin by inducing activation of JNK/mitochondrial pathway but not ERK and p-38 pathways, suggesting critical roles of TWIST in A549 cell chemoresistance to cisplatin and raising the possibility of TWIST depletion as a promising approach to lung cancer therapy. Cisplatin 236-245 mitogen-activated protein kinase 8 Homo sapiens 112-115 18249159-7 2008 Knock-down of ATF3 and Fra1 results in increased and decreased cisplatin-induced apoptosis, respectively, indicating that ATF3 is an anti-apoptotic JNK effector and Fra1 is a pro-apoptotic ERK/JNK effector. Cisplatin 63-72 mitogen-activated protein kinase 8 Homo sapiens 148-151 18249159-7 2008 Knock-down of ATF3 and Fra1 results in increased and decreased cisplatin-induced apoptosis, respectively, indicating that ATF3 is an anti-apoptotic JNK effector and Fra1 is a pro-apoptotic ERK/JNK effector. Cisplatin 63-72 mitogen-activated protein kinase 8 Homo sapiens 193-196 18249159-4 2008 We show that the anti-cancer drug cisplatin or UV light activates both JNK and ERK in human glioblastoma cells lacking functional p53. Cisplatin 34-43 mitogen-activated protein kinase 8 Homo sapiens 71-74 18249159-5 2008 Inhibition experiments of JNK or ERK activities revealed that the ERK pathway strongly promotes cisplatin- and UV-induced apoptosis in these glioblastoma cells. Cisplatin 96-105 mitogen-activated protein kinase 8 Homo sapiens 26-29 18249159-6 2008 Furthermore, JNK but not ERK is required for ATF3 induction, and both ERK and JNK are necessary for post-transcriptional induction of Fra1 in response to cisplatin or UV. Cisplatin 154-163 mitogen-activated protein kinase 8 Homo sapiens 78-81 17418561-8 2007 These results demonstrate that the expression of HO-1 by piperine is mediated by both JNK pathway and Nrf2, and the expression inhibits cisplatin-induced apoptosis in HEI-OC1 cells. Cisplatin 136-145 mitogen-activated protein kinase 8 Homo sapiens 86-89 18093981-1 2008 In response to diverse genotoxic stimuli (e.g. UV and cisplatin), the mitogen-activated protein kinases ERK1/2, JNK1/2, and p38alpha/beta become rapidly phosphorylated and in turn activate multiple downstream effectors that modulate apoptosis and/or growth arrest. Cisplatin 54-63 mitogen-activated protein kinase 8 Homo sapiens 112-118 16984892-8 2006 In addition, sustained activation of the JNK1 pathway by cisplatin similarly triggered CtBP degradation. Cisplatin 57-66 mitogen-activated protein kinase 8 Homo sapiens 41-45 17586463-0 2007 Epstein-Barr virus-encoded LMP1 promotes cisplatin-induced caspase activation through JNK and NF-kappaB signaling pathways. Cisplatin 41-50 mitogen-activated protein kinase 8 Homo sapiens 86-89 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 mitogen-activated protein kinase 8 Homo sapiens 29-52 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 mitogen-activated protein kinase 8 Homo sapiens 127-130 17283157-9 2007 SP600125, an inhibitor of JNK, or antioxidant N-acetyl-L-cysteine inhibited the enhancement of chemosensitivity against CDDP by galectin-7 transfection. Cisplatin 120-124 mitogen-activated protein kinase 8 Homo sapiens 26-29 17409444-10 2007 Consequently, an inhibitor of JNK/SAPK decreased the sensitivity of pancreatic cancer cells to apoptosis by glucose deprivation and CDDP. Cisplatin 132-136 mitogen-activated protein kinase 8 Homo sapiens 30-38 16529740-3 2006 When human melanoma cells were treated with cisplatin, Bak function was found to be regulated in two distinct steps by two SAP kinases, MEKK1 and JNK1. Cisplatin 44-53 mitogen-activated protein kinase 8 Homo sapiens 146-150 16951204-9 2006 More importantly, cisplatin-induced cell death is inhibited by blocking JNK but not ERK and p38 activities. Cisplatin 18-27 mitogen-activated protein kinase 8 Homo sapiens 72-75 16951204-10 2006 Collectively, our results establish a critical role of JNK in cisplatin-induced apoptosis and suggest that MKP-1 is required for cisplatin resistance. Cisplatin 62-71 mitogen-activated protein kinase 8 Homo sapiens 55-58 16462770-3 2006 Cisplatin, a commonly used therapeutic agent in NSCLC, induces activation of N-terminal-c-Jun kinase (JNK) that, in turn, mediates induction of apoptosis. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 77-100 16462770-3 2006 Cisplatin, a commonly used therapeutic agent in NSCLC, induces activation of N-terminal-c-Jun kinase (JNK) that, in turn, mediates induction of apoptosis. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 102-105 16462770-6 2006 Expressing a small-interfering RNA (siRNA) vector for MKP1 in H-460 cells resulted in a more efficient activation by cisplatin of JNK and p38 than in the parental cells, and this correlated with a 10-fold increase in sensitivity to cisplatin. Cisplatin 117-126 mitogen-activated protein kinase 8 Homo sapiens 130-133 16596182-5 2006 Our results suggest that the ability of CDDP to kill these cells can be mediated by JNK, p38 MAPK and ROS, but not by ERK. Cisplatin 40-44 mitogen-activated protein kinase 8 Homo sapiens 84-87 16596182-8 2006 Therefore, the JNK pathway appears to be an ideal target for the modulation of the lethal action of CDDP in multiple types of p53-mutated cells. Cisplatin 100-104 mitogen-activated protein kinase 8 Homo sapiens 15-18 16518417-6 2006 Furthermore, inhibition of JNK, using SP600125, completely suppressed activity of caspases and poly-(ADP-ribose) polymerase cleavage, leading to suppression of enhancement of CDDP-mediated apoptosis by dicoumarol. Cisplatin 175-179 mitogen-activated protein kinase 8 Homo sapiens 27-30 16518417-7 2006 These results suggested that dicoumarol could enhance cytotoxicity of CDDP in urogenital cancer cells with wild-type p53 through the p53/p21/JNK pathways. Cisplatin 70-74 mitogen-activated protein kinase 8 Homo sapiens 141-144 16518417-0 2006 Dicoumarol potentiates cisplatin-induced apoptosis mediated by c-Jun N-terminal kinase in p53 wild-type urogenital cancer cell lines. Cisplatin 23-32 mitogen-activated protein kinase 8 Homo sapiens 63-86 16619517-2 2006 DNA-damaging agents, such as CDDP induced sustained activation of c-Jun N-terminal kinase (JNK), probably leading to apoptosis. Cisplatin 29-33 mitogen-activated protein kinase 8 Homo sapiens 66-89 16619517-2 2006 DNA-damaging agents, such as CDDP induced sustained activation of c-Jun N-terminal kinase (JNK), probably leading to apoptosis. Cisplatin 29-33 mitogen-activated protein kinase 8 Homo sapiens 91-94 16619517-3 2006 In the present study, whether JNK activation is involved in apoptotic cell death induced by combined treatment with CDDP/DXR and TRAIL was addressed. Cisplatin 116-120 mitogen-activated protein kinase 8 Homo sapiens 30-33 16619517-6 2006 Interestingly, partial inhibition of the cell death induced by the combined treatment with CDDP/DXR and TRAIL was found in MG-63 or SaOS-2 cells overexpressing dnJNK1, suggesting that JNK activation is required for the combined treatment. Cisplatin 91-95 mitogen-activated protein kinase 8 Homo sapiens 162-165 16619517-8 2006 CONCLUSION: Efficient cell death induced by combined treatment with the chemotherapeutic agents CDDP/DXR and TRAIL is involved in JNK activation in the sarcoma cell lines MG-63 and SaOS-2. Cisplatin 96-100 mitogen-activated protein kinase 8 Homo sapiens 130-133 16357177-6 2005 Importantly, combined therapy with bortezomib plus cisplatin induced JNK activation and apoptosis in orthotopic pancreatic tumors resulting in a reduction in tumor burden. Cisplatin 51-60 mitogen-activated protein kinase 8 Homo sapiens 69-72 16038800-6 2005 Furthermore, whilst pre-treatment of cells with either the JNK inhibitor SP600125, or the MEK-1 inhibitor PD98059, also reverses UV-C and cisplatin-induced apoptosis, the anti-apoptotic effect of MKP-2 overexpression is not additive with SP600125 but is with PD098059, suggesting that MKP-2 is involved in specifically terminating JNK activity and not ERK. Cisplatin 138-147 mitogen-activated protein kinase 8 Homo sapiens 59-62 16105650-0 2005 Reversing chemoresistance in cisplatin-resistant human ovarian cancer cells: a role of c-Jun NH2-terminal kinase 1. Cisplatin 29-38 mitogen-activated protein kinase 8 Homo sapiens 87-114 16105650-1 2005 To investigate the role of activation of c-Jun NH2-terminal kinase 1 (JNK1) in mediating cisplatin-induced apoptosis and the possibility of induction of JNK activity in triggering relation to DNA damage and drug resistance. Cisplatin 89-98 mitogen-activated protein kinase 8 Homo sapiens 41-68 16105650-1 2005 To investigate the role of activation of c-Jun NH2-terminal kinase 1 (JNK1) in mediating cisplatin-induced apoptosis and the possibility of induction of JNK activity in triggering relation to DNA damage and drug resistance. Cisplatin 89-98 mitogen-activated protein kinase 8 Homo sapiens 70-74 16105650-1 2005 To investigate the role of activation of c-Jun NH2-terminal kinase 1 (JNK1) in mediating cisplatin-induced apoptosis and the possibility of induction of JNK activity in triggering relation to DNA damage and drug resistance. Cisplatin 89-98 mitogen-activated protein kinase 8 Homo sapiens 70-73 16105650-2 2005 We investigated the difference of cisplatin-induced activation of JNK pathway and H2O2 alteration between cisplatin-sensitive human ovarian carcinoma cell line A2780 and its resistant variant A2780/DDP. Cisplatin 34-43 mitogen-activated protein kinase 8 Homo sapiens 66-69 16105650-4 2005 Both A2780 and A2780/DDP were treated with CDDP, the JNK pathway was activated and a prolonged JNK activation was maintained for at least 12 h in A2780, and only a transient activation (3 h) was detected in A2780/DDP in response to cisplatin treatment. Cisplatin 43-47 mitogen-activated protein kinase 8 Homo sapiens 53-56 16105650-4 2005 Both A2780 and A2780/DDP were treated with CDDP, the JNK pathway was activated and a prolonged JNK activation was maintained for at least 12 h in A2780, and only a transient activation (3 h) was detected in A2780/DDP in response to cisplatin treatment. Cisplatin 43-47 mitogen-activated protein kinase 8 Homo sapiens 95-98 16105650-5 2005 Inhibition of JNK activity by transfection with a dominant negative allele of JNK blocked CDDP-induced apoptosis significantly in A2780 cells. Cisplatin 90-94 mitogen-activated protein kinase 8 Homo sapiens 14-17 16105650-5 2005 Inhibition of JNK activity by transfection with a dominant negative allele of JNK blocked CDDP-induced apoptosis significantly in A2780 cells. Cisplatin 90-94 mitogen-activated protein kinase 8 Homo sapiens 78-81 16105650-6 2005 Selective stimulation of the JNK pathway by lipofectamine-mediated delivery of recombinant JNK1 led to activation of c-Jun and decrease of extracellular H2O2, as well as apoptosis sensitization to CDDP in A2780/DDP cells. Cisplatin 197-201 mitogen-activated protein kinase 8 Homo sapiens 29-32 16105650-6 2005 Selective stimulation of the JNK pathway by lipofectamine-mediated delivery of recombinant JNK1 led to activation of c-Jun and decrease of extracellular H2O2, as well as apoptosis sensitization to CDDP in A2780/DDP cells. Cisplatin 197-201 mitogen-activated protein kinase 8 Homo sapiens 91-95 16105650-7 2005 We concluded that JNK pathway might play an important role in mediating cisplatin-induced apoptosis in A2780 cells, and the duration of JNK activation might be critical in determining whether cells survive or undergo apoptosis. Cisplatin 72-81 mitogen-activated protein kinase 8 Homo sapiens 18-21 16105650-8 2005 The resistance to CDDP can be reversed through activating c-Jun and decreasing extracellular generation of H2O2 by pcDNA3(FLAG)-JNK1-wt transfection in A2780/DDP cells. Cisplatin 18-22 mitogen-activated protein kinase 8 Homo sapiens 128-132 16038800-6 2005 Furthermore, whilst pre-treatment of cells with either the JNK inhibitor SP600125, or the MEK-1 inhibitor PD98059, also reverses UV-C and cisplatin-induced apoptosis, the anti-apoptotic effect of MKP-2 overexpression is not additive with SP600125 but is with PD098059, suggesting that MKP-2 is involved in specifically terminating JNK activity and not ERK. Cisplatin 138-147 mitogen-activated protein kinase 8 Homo sapiens 331-334 15841377-4 2005 We used NER-deficient human fibroblasts to study the role of DNA damage in the activation of JNK and cell death following cisplatin treatment. Cisplatin 122-131 mitogen-activated protein kinase 8 Homo sapiens 93-96 16082193-8 2005 Cisplatin induced apoptosis appears to be partly due to induction of JNK activity which leads to the activation of endonucleases. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 69-72 15841377-6 2005 RESULTS: Cisplatin induced a transient increase in JNK-1 activity of about tenfold in normal and XP-C fibroblasts, which declined to about two- to threefold 24 h after treatment. Cisplatin 9-18 mitogen-activated protein kinase 8 Homo sapiens 51-56 15841377-7 2005 In contrast, the activation of JNK-1 was persistent in XP-A and CS fibroblasts at 24 h after treatment and CS cells and XP-A cells, but not XP-C cells, were more sensitive to cisplatin than normal cells. Cisplatin 175-184 mitogen-activated protein kinase 8 Homo sapiens 31-36 15841377-9 2005 Further, it is this amplified and prolonged JNK activation that correlates with cisplatin-induced cell death. Cisplatin 80-89 mitogen-activated protein kinase 8 Homo sapiens 44-47 15386344-7 2004 cDDP provoked the activation of stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) and p38 kinase dose-dependently, with significantly lower levels in ACR cells than in the sensitive parental line. Cisplatin 0-4 mitogen-activated protein kinase 8 Homo sapiens 94-97 16238095-4 2005 We have investigated the regulation of the JNK-1 kinase by co-transfecting phosphatases PP4 and M3/6 in prostate cancer cell lines PC-3 and LNCaP, which have been previously stimulated with human EGF or cisplatin. Cisplatin 203-212 mitogen-activated protein kinase 8 Homo sapiens 43-48 15386344-0 2004 Long-term activation of SAPK/JNK, p38 kinase and fas-L expression by cisplatin is attenuated in human carcinoma cells that acquired drug resistance. Cisplatin 69-78 mitogen-activated protein kinase 8 Homo sapiens 29-32 15386344-10 2004 Inhibition of either JNK or p38 kinase (by JNK inhibitor II and SB 203580, respectively) attenuated cDDP-induced apoptosis, supporting the role of JNK and p38 kinase in the cDDP response. Cisplatin 100-104 mitogen-activated protein kinase 8 Homo sapiens 21-24 15386344-10 2004 Inhibition of either JNK or p38 kinase (by JNK inhibitor II and SB 203580, respectively) attenuated cDDP-induced apoptosis, supporting the role of JNK and p38 kinase in the cDDP response. Cisplatin 100-104 mitogen-activated protein kinase 8 Homo sapiens 43-46 15386344-10 2004 Inhibition of either JNK or p38 kinase (by JNK inhibitor II and SB 203580, respectively) attenuated cDDP-induced apoptosis, supporting the role of JNK and p38 kinase in the cDDP response. Cisplatin 100-104 mitogen-activated protein kinase 8 Homo sapiens 43-46 15386344-10 2004 Inhibition of either JNK or p38 kinase (by JNK inhibitor II and SB 203580, respectively) attenuated cDDP-induced apoptosis, supporting the role of JNK and p38 kinase in the cDDP response. Cisplatin 173-177 mitogen-activated protein kinase 8 Homo sapiens 21-24 15386344-11 2004 Since several independently derived cDDP-resistant cell lines displayed attenuated MAPK signaling, sustained SAPK/JNK and p38 kinase activation may be a general mechanism of cDDP-induced cell death. Cisplatin 36-40 mitogen-activated protein kinase 8 Homo sapiens 114-117 15386344-11 2004 Since several independently derived cDDP-resistant cell lines displayed attenuated MAPK signaling, sustained SAPK/JNK and p38 kinase activation may be a general mechanism of cDDP-induced cell death. Cisplatin 174-178 mitogen-activated protein kinase 8 Homo sapiens 114-117 15386344-12 2004 ACR cells displayed a reduced level of DNA damage, indicating long-term stimulation of SAPK/JNK and p38 kinase is triggered by nonrepaired cDDP-induced DNA lesions. Cisplatin 139-143 mitogen-activated protein kinase 8 Homo sapiens 92-95 15604295-10 2004 Although the stress-activated protein kinase/c-Jun NH(2)-terminal kinase (JNK) signaling pathway is activated in response to CDDP toxicity, intracochlear perfusion of d-JNKI-1, a JNK inhibitor, did not protect against CDDP ototoxicity but instead potentiated the ototoxic effects of CDDP. Cisplatin 125-129 mitogen-activated protein kinase 8 Homo sapiens 74-77 12697749-4 2003 Here we demonstrate that constitutively active AKT2 renders cisplatin-sensitive A2780S ovarian cancer cells resistant to cisplatin, whereas phosphatidylinositol 3-kinase inhibitor or dominant negative AKT2 sensitizes A2780S and cisplatin-resistant A2780CP cells to cisplatin-induced apoptosis through regulation of the ASK1/JNK/p38 pathway. Cisplatin 60-69 mitogen-activated protein kinase 8 Homo sapiens 324-327 15254743-8 2004 Finally, the compound was found to block cisplatin-induced increases in AP-1 expression and JNK activity, as well as Raf-1 protein level in these cells. Cisplatin 41-50 mitogen-activated protein kinase 8 Homo sapiens 92-95 15001534-5 2004 It is noteworthy that pretreatment with paclitaxel significantly up-regulated MEKK1 expression, resulting in enhancement of etoposide- or cisplatin-induced MEKK1/MKK7-dependent JNK activation and apoptosis in LNCaP and DU145 cells. Cisplatin 138-147 mitogen-activated protein kinase 8 Homo sapiens 177-180 14520687-3 2003 Inhibition of JNK activity delayed the onset of apoptosis induced by cisplatin, doxorubicin, gamma-irradiation and CD95-L but did not prevent apoptosis per se. Cisplatin 69-78 mitogen-activated protein kinase 8 Homo sapiens 14-17 14722256-4 2004 Analysis of signaling pathways revealed that cisplatin-induced activation of c-Jun N-terminal kinase (JNK) was fully blocked by 17-AAG in HT-29 and SW480 cells, whereas in HCT 116 and DLD1 cells it was inhibited only partially. Cisplatin 45-54 mitogen-activated protein kinase 8 Homo sapiens 77-100 14722256-4 2004 Analysis of signaling pathways revealed that cisplatin-induced activation of c-Jun N-terminal kinase (JNK) was fully blocked by 17-AAG in HT-29 and SW480 cells, whereas in HCT 116 and DLD1 cells it was inhibited only partially. Cisplatin 45-54 mitogen-activated protein kinase 8 Homo sapiens 102-105 14722256-8 2004 Alternatively, sustained activation of JNK pathway led to an increase of the cytotoxicity of the cisplatin/17-AAG combination in HT-29 cells. Cisplatin 97-106 mitogen-activated protein kinase 8 Homo sapiens 39-42 14722256-9 2004 Taken together, these data suggest that the synergistic interaction of this combination in colon cancer cell lines depends on the effect exerted by 17-AAG on cisplatin-induced signaling through JNK and associated pathways leading to cell death. Cisplatin 158-167 mitogen-activated protein kinase 8 Homo sapiens 194-197 12697749-0 2003 AKT2 inhibition of cisplatin-induced JNK/p38 and Bax activation by phosphorylation of ASK1: implication of AKT2 in chemoresistance. Cisplatin 19-28 mitogen-activated protein kinase 8 Homo sapiens 37-40 12697749-8 2003 Cisplatin-induced Bax conformation change was inhibited by inhibitors or dominant negative forms of JNK and p38. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 100-103 12697749-9 2003 In conclusion, our data indicate that AKT2 inhibits cisplatin-induced JNK/p38 and Bax activation through phosphorylation of ASK1 and thus, plays an important role in chemoresistance. Cisplatin 52-61 mitogen-activated protein kinase 8 Homo sapiens 70-73 12181446-2 2002 In this study, we tested the role of the c-Jun N-terminal kinase (JNK) family of mitogen-activated protein kinases and their transcription factor target, c-Jun, in the cytotoxic response of small-cell lung cancer (SCLC) cells to cisplatin and its less effective trans-isomer, transplatin. Cisplatin 229-238 mitogen-activated protein kinase 8 Homo sapiens 41-64 12663670-3 2003 We have observed that four DNA-damaging agents (cisplatin, actinomycin D, MMS, and etoposide), but not the cisplatin isomer, transplatin, which does not readily damage DNA, strongly activate JNK, p38, and extracellular signal-regulated kinase (ERK), and strongly increase phosphorylation and ATF2-dependent transcriptional activity. Cisplatin 48-57 mitogen-activated protein kinase 8 Homo sapiens 191-194 12637505-10 2003 Thus, the JNK > c-Jun > FasL > Fas pathway plays an important role in mediating cisplatin-induced apoptosis in ovarian cancer cells, and the duration of JNK activation is critical in determining whether cells survive or undergo apoptosis. Cisplatin 89-98 mitogen-activated protein kinase 8 Homo sapiens 10-13 12637505-10 2003 Thus, the JNK > c-Jun > FasL > Fas pathway plays an important role in mediating cisplatin-induced apoptosis in ovarian cancer cells, and the duration of JNK activation is critical in determining whether cells survive or undergo apoptosis. Cisplatin 89-98 mitogen-activated protein kinase 8 Homo sapiens 162-165 12637505-0 2003 Sustained activation of JNK/p38 MAPK pathways in response to cisplatin leads to Fas ligand induction and cell death in ovarian carcinoma cells. Cisplatin 61-70 mitogen-activated protein kinase 8 Homo sapiens 24-27 12637505-4 2003 We compared cisplatin-induced activation of three MAPKs, JNK, p38, and ERK, in a cisplatin-sensitive human ovarian carcinoma cell line (2008) and its resistant subclone (2008C13). Cisplatin 12-21 mitogen-activated protein kinase 8 Homo sapiens 57-60 12637505-5 2003 The JNK and p38 pathways were activated differentially in response to cisplatin, with the cisplatin-sensitive cells showing prolonged activation (8-12 h) and the cisplatin-resistant cells showing only transient activation (1-3 h) of JNK and p38. Cisplatin 70-79 mitogen-activated protein kinase 8 Homo sapiens 4-7 12637505-5 2003 The JNK and p38 pathways were activated differentially in response to cisplatin, with the cisplatin-sensitive cells showing prolonged activation (8-12 h) and the cisplatin-resistant cells showing only transient activation (1-3 h) of JNK and p38. Cisplatin 70-79 mitogen-activated protein kinase 8 Homo sapiens 233-236 12637505-5 2003 The JNK and p38 pathways were activated differentially in response to cisplatin, with the cisplatin-sensitive cells showing prolonged activation (8-12 h) and the cisplatin-resistant cells showing only transient activation (1-3 h) of JNK and p38. Cisplatin 90-99 mitogen-activated protein kinase 8 Homo sapiens 4-7 12637505-5 2003 The JNK and p38 pathways were activated differentially in response to cisplatin, with the cisplatin-sensitive cells showing prolonged activation (8-12 h) and the cisplatin-resistant cells showing only transient activation (1-3 h) of JNK and p38. Cisplatin 90-99 mitogen-activated protein kinase 8 Homo sapiens 233-236 12637505-5 2003 The JNK and p38 pathways were activated differentially in response to cisplatin, with the cisplatin-sensitive cells showing prolonged activation (8-12 h) and the cisplatin-resistant cells showing only transient activation (1-3 h) of JNK and p38. Cisplatin 90-99 mitogen-activated protein kinase 8 Homo sapiens 4-7 12637505-5 2003 The JNK and p38 pathways were activated differentially in response to cisplatin, with the cisplatin-sensitive cells showing prolonged activation (8-12 h) and the cisplatin-resistant cells showing only transient activation (1-3 h) of JNK and p38. Cisplatin 90-99 mitogen-activated protein kinase 8 Homo sapiens 233-236 12637505-6 2003 In the sensitive cells, inhibition of cisplatin-induced JNK and p38 activation blocked cisplatin-induced apoptosis; persistent activation of JNK resulted in hyperphosphorylation of the c-Jun transcription factor, which in turn stimulated the transcription of an immediate downstream target, the death inducer Fas ligand (FasL). Cisplatin 38-47 mitogen-activated protein kinase 8 Homo sapiens 56-59 12637505-6 2003 In the sensitive cells, inhibition of cisplatin-induced JNK and p38 activation blocked cisplatin-induced apoptosis; persistent activation of JNK resulted in hyperphosphorylation of the c-Jun transcription factor, which in turn stimulated the transcription of an immediate downstream target, the death inducer Fas ligand (FasL). Cisplatin 87-96 mitogen-activated protein kinase 8 Homo sapiens 56-59 12181446-2 2002 In this study, we tested the role of the c-Jun N-terminal kinase (JNK) family of mitogen-activated protein kinases and their transcription factor target, c-Jun, in the cytotoxic response of small-cell lung cancer (SCLC) cells to cisplatin and its less effective trans-isomer, transplatin. Cisplatin 229-238 mitogen-activated protein kinase 8 Homo sapiens 66-69 12181446-3 2002 Both agents stimulated JNK activity; the transplatin response was rapid and transient, whereas JNK activation by cisplatin was delayed and sustained. Cisplatin 113-122 mitogen-activated protein kinase 8 Homo sapiens 95-98 12181446-4 2002 Despite the differential kinetics of JNK activation, expression of nonphosphorylatable JNK mutants sensitized the SCLC cells to killing by cisplatin or transplatin, suggesting that JNK activation in response to these agents signals a protective response. Cisplatin 139-148 mitogen-activated protein kinase 8 Homo sapiens 87-90 12181446-4 2002 Despite the differential kinetics of JNK activation, expression of nonphosphorylatable JNK mutants sensitized the SCLC cells to killing by cisplatin or transplatin, suggesting that JNK activation in response to these agents signals a protective response. Cisplatin 139-148 mitogen-activated protein kinase 8 Homo sapiens 87-90 11592233-9 2001 JNK activity was decreased by 1.8-fold, as well as the expression of its downstream target c-jun (1.9-fold), when tumor cells were exposed to cisplatin in the presence of nicotine. Cisplatin 142-151 mitogen-activated protein kinase 8 Homo sapiens 0-3 12018840-0 2002 Signaling and function of caspase and c-jun N-terminal kinase in cisplatin-induced apoptosis. Cisplatin 65-74 mitogen-activated protein kinase 8 Homo sapiens 38-61 12018840-3 2002 Treatment of Jurkat T-cells with cisplatin induced cell death with DNA fragmentation and activation of caspase and JNK. Cisplatin 33-42 mitogen-activated protein kinase 8 Homo sapiens 115-118 12018840-7 2002 On the other hand, cisplatin induced the JNK activation in both the wild-type and JB-6 cells, and the caspase-3 inhibitor Z-DEVD-fmk did not inhibit this activation. Cisplatin 19-28 mitogen-activated protein kinase 8 Homo sapiens 41-44 12018840-8 2002 The JNK overexpression resulted in a higher JNK activity, AP-1 DNA binding activity, and metallothionein expression than the empty vector-transfected cells following cisplatin treatment. Cisplatin 166-175 mitogen-activated protein kinase 8 Homo sapiens 4-7 12018840-10 2002 These data suggest that the cisplatin-induced apoptotic signal is initiated by the caspase-8-independent cytochrome c release, and the JNK activation protects cells from cisplatin-induced apoptosis via the metallothionein expression. Cisplatin 170-179 mitogen-activated protein kinase 8 Homo sapiens 135-138 30147474-0 2001 Activation of the JNK/SAPK and P38 Mitogen-Activated Protein Kinase Signaling Pathways Sensitize Tumor Cells to Cisplatin-Induced Apoptosis. Cisplatin 112-121 mitogen-activated protein kinase 8 Homo sapiens 18-21 12149148-6 2002 When CDDP and an anti-GD2 mAb were used together, significantly stronger JNK activation was observed corresponding to the cytotoxic effects, suggesting that synergistic phosphorylation of JNK with two reagents induced prominent apoptosis. Cisplatin 5-9 mitogen-activated protein kinase 8 Homo sapiens 73-76 12149148-6 2002 When CDDP and an anti-GD2 mAb were used together, significantly stronger JNK activation was observed corresponding to the cytotoxic effects, suggesting that synergistic phosphorylation of JNK with two reagents induced prominent apoptosis. Cisplatin 5-9 mitogen-activated protein kinase 8 Homo sapiens 188-191 12149148-7 2002 The essential role of JNK in the induction of SCLC apoptosis with CDDP and anti-GD2 mAb was confirmed by experiments with a JNK inhibitor, curcumin. Cisplatin 66-70 mitogen-activated protein kinase 8 Homo sapiens 22-25 11340162-9 2001 In summary, we have identified Bak as a cisplatin-regulated component downstream in a proapoptotic, JNK-independent DeltaMEKK1 pathway. Cisplatin 40-49 mitogen-activated protein kinase 8 Homo sapiens 100-103 11396136-17 2001 The reduction of CDDP-induced apoptosis under glucose-starved stress condition was influenced by JNK1/SAPK and caspase-3 proteins. Cisplatin 17-21 mitogen-activated protein kinase 8 Homo sapiens 97-101 10531373-0 1999 Inhibition of extracellular signal-regulated protein kinase or c-Jun N-terminal protein kinase cascade, differentially activated by cisplatin, sensitizes human ovarian cancer cell line. Cisplatin 132-141 mitogen-activated protein kinase 8 Homo sapiens 63-94 11170260-3 2000 Dose-dependent and time-dependent activation of JNK1 and ERK1/2 occurred in each of the three cell lines in response to cisplatin treatment. Cisplatin 120-129 mitogen-activated protein kinase 8 Homo sapiens 48-52 11170260-4 2000 The requirement of higher concentrations of cisplatin for induction of maximum activation of JNK1 and ERK1/2 was correlated with increased levels of cisplatin resistance. Cisplatin 44-53 mitogen-activated protein kinase 8 Homo sapiens 93-97 11170260-4 2000 The requirement of higher concentrations of cisplatin for induction of maximum activation of JNK1 and ERK1/2 was correlated with increased levels of cisplatin resistance. Cisplatin 149-158 mitogen-activated protein kinase 8 Homo sapiens 93-97 11170260-7 2000 In conclusion, different patterns of cisplatin-induced JNK1 and ERK1/2 activation are observed in cell lines with different levels of cisplatin sensitivity, and inhibition of cisplatin-induced ERK1/2 activation enhances sensitivity to cisplatin in both cisplatin-sensitive and cisplatin-resistant cell lines. Cisplatin 37-46 mitogen-activated protein kinase 8 Homo sapiens 55-59 11170260-7 2000 In conclusion, different patterns of cisplatin-induced JNK1 and ERK1/2 activation are observed in cell lines with different levels of cisplatin sensitivity, and inhibition of cisplatin-induced ERK1/2 activation enhances sensitivity to cisplatin in both cisplatin-sensitive and cisplatin-resistant cell lines. Cisplatin 134-143 mitogen-activated protein kinase 8 Homo sapiens 55-59 11170260-7 2000 In conclusion, different patterns of cisplatin-induced JNK1 and ERK1/2 activation are observed in cell lines with different levels of cisplatin sensitivity, and inhibition of cisplatin-induced ERK1/2 activation enhances sensitivity to cisplatin in both cisplatin-sensitive and cisplatin-resistant cell lines. Cisplatin 134-143 mitogen-activated protein kinase 8 Homo sapiens 55-59 11170260-7 2000 In conclusion, different patterns of cisplatin-induced JNK1 and ERK1/2 activation are observed in cell lines with different levels of cisplatin sensitivity, and inhibition of cisplatin-induced ERK1/2 activation enhances sensitivity to cisplatin in both cisplatin-sensitive and cisplatin-resistant cell lines. Cisplatin 134-143 mitogen-activated protein kinase 8 Homo sapiens 55-59 11170260-7 2000 In conclusion, different patterns of cisplatin-induced JNK1 and ERK1/2 activation are observed in cell lines with different levels of cisplatin sensitivity, and inhibition of cisplatin-induced ERK1/2 activation enhances sensitivity to cisplatin in both cisplatin-sensitive and cisplatin-resistant cell lines. Cisplatin 134-143 mitogen-activated protein kinase 8 Homo sapiens 55-59 11170260-7 2000 In conclusion, different patterns of cisplatin-induced JNK1 and ERK1/2 activation are observed in cell lines with different levels of cisplatin sensitivity, and inhibition of cisplatin-induced ERK1/2 activation enhances sensitivity to cisplatin in both cisplatin-sensitive and cisplatin-resistant cell lines. Cisplatin 134-143 mitogen-activated protein kinase 8 Homo sapiens 55-59 11064451-0 2000 CL100/MKP-1 modulates JNK activation and apoptosis in response to cisplatin. Cisplatin 66-75 mitogen-activated protein kinase 8 Homo sapiens 22-25 11064451-1 2000 Treatment of cells with cisplatin induces a sustained activation of the stress activated protein kinase SAPK/JNK and the mitogen-activated protein kinase p38. Cisplatin 24-33 mitogen-activated protein kinase 8 Homo sapiens 109-112 11064451-2 2000 Activation of JNK by cisplatin is necessary for the induction of apoptosis. Cisplatin 21-30 mitogen-activated protein kinase 8 Homo sapiens 14-17 11064451-3 2000 Expression of the MAPK phosphatases CL100/MKP-1 and hVH-5 selectively prevents JNK/SAPK activation by cisplatin in a dose dependent fashion and results in protection against cisplatin-induced apoptosis. Cisplatin 102-111 mitogen-activated protein kinase 8 Homo sapiens 79-82 11170260-0 2000 Cisplatin-induced response of c-jun N-terminal kinase 1 and extracellular signal--regulated protein kinases 1 and 2 in a series of cisplatin-resistant ovarian carcinoma cell lines. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 30-55 11170260-0 2000 Cisplatin-induced response of c-jun N-terminal kinase 1 and extracellular signal--regulated protein kinases 1 and 2 in a series of cisplatin-resistant ovarian carcinoma cell lines. Cisplatin 131-140 mitogen-activated protein kinase 8 Homo sapiens 30-55 11170260-2 2000 In this study, we compared the cisplatin-induced activation of two MAP kinases, c-jun N-terminal kinase 1 (JNK1) and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), in the cisplatin-sensitive ovarian carcinoma cell line A2780 and its derivative cisplatin-resistant cell lines CP70 and C200. Cisplatin 31-40 mitogen-activated protein kinase 8 Homo sapiens 80-105 11170260-2 2000 In this study, we compared the cisplatin-induced activation of two MAP kinases, c-jun N-terminal kinase 1 (JNK1) and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), in the cisplatin-sensitive ovarian carcinoma cell line A2780 and its derivative cisplatin-resistant cell lines CP70 and C200. Cisplatin 31-40 mitogen-activated protein kinase 8 Homo sapiens 107-111 11170260-2 2000 In this study, we compared the cisplatin-induced activation of two MAP kinases, c-jun N-terminal kinase 1 (JNK1) and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), in the cisplatin-sensitive ovarian carcinoma cell line A2780 and its derivative cisplatin-resistant cell lines CP70 and C200. Cisplatin 189-198 mitogen-activated protein kinase 8 Homo sapiens 80-105 11170260-2 2000 In this study, we compared the cisplatin-induced activation of two MAP kinases, c-jun N-terminal kinase 1 (JNK1) and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), in the cisplatin-sensitive ovarian carcinoma cell line A2780 and its derivative cisplatin-resistant cell lines CP70 and C200. Cisplatin 189-198 mitogen-activated protein kinase 8 Homo sapiens 107-111 11170260-2 2000 In this study, we compared the cisplatin-induced activation of two MAP kinases, c-jun N-terminal kinase 1 (JNK1) and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), in the cisplatin-sensitive ovarian carcinoma cell line A2780 and its derivative cisplatin-resistant cell lines CP70 and C200. Cisplatin 189-198 mitogen-activated protein kinase 8 Homo sapiens 80-105 11170260-2 2000 In this study, we compared the cisplatin-induced activation of two MAP kinases, c-jun N-terminal kinase 1 (JNK1) and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), in the cisplatin-sensitive ovarian carcinoma cell line A2780 and its derivative cisplatin-resistant cell lines CP70 and C200. Cisplatin 189-198 mitogen-activated protein kinase 8 Homo sapiens 107-111 10639576-4 2000 In this report, we show that cisplatin activates a robust apoptotic pathway involving the activation of JNK and p38MAPK whereas it fails to elicit such a response in cisplatin-resistant 2008/C13 cells. Cisplatin 29-38 mitogen-activated protein kinase 8 Homo sapiens 104-107 10531373-2 1999 Treatment of both cells with cisplatin but not transplatin isomer activates JNK and ERK. Cisplatin 29-38 mitogen-activated protein kinase 8 Homo sapiens 76-79 10531373-3 1999 Activation of JNK by cisplatin occurred at 30 min, reached a plateau at 3 h, and declined thereafter, whereas activation of ERK by cisplatin showed a biphasic pattern, indicating the different time frame. Cisplatin 21-30 mitogen-activated protein kinase 8 Homo sapiens 14-17 10531373-4 1999 Activation of JNK by cisplatin was maximal at 1000 microM, whereas activation of ERK was maximal at 100 microM and was less at higher concentrations, indicating the different dose dependence. Cisplatin 21-30 mitogen-activated protein kinase 8 Homo sapiens 14-17 10531373-5 1999 Cisplatin-induced JNK activation was neither extracellular and intracellular Ca(2+)- nor protein kinase C-dependent, whereas cisplatin-induced ERK activation was extracellular and intracellular Ca(2+)- dependent and protein kinase C-dependent. Cisplatin 0-9 mitogen-activated protein kinase 8 Homo sapiens 18-21 10531373-9 1999 Our findings suggest that cisplatin-induced DNA damage differentially activates JNK and ERK cascades and that inhibition of either of these cascades sensitizes ovarian cancer cells to cisplatin. Cisplatin 26-35 mitogen-activated protein kinase 8 Homo sapiens 80-83