PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 14 Homo sapiens 68-71 34008860-0 2021 Resveratrol inhibited the metastatic behaviors of cisplatin-resistant human oral cancer cells via phosphorylation of ERK/p-38 and suppression of MMP-2/9. Cisplatin 50-59 mitogen-activated protein kinase 14 Homo sapiens 121-125 32252293-6 2020 Upon cisplatin treatment, CD44v6+ cells survive better and have lower apoptosis levels than CD44v6- cells, possibly due to concomitant activation of STAT3 and P38. Cisplatin 5-14 mitogen-activated protein kinase 14 Homo sapiens 159-162 33302041-0 2021 p38 Mitogen-activated protein kinase modulates cisplatin resistance in Head and Neck Squamous Cell Carcinoma cells. Cisplatin 47-56 mitogen-activated protein kinase 14 Homo sapiens 0-36 33302041-1 2021 OBJECTIVE: This study aims to investigate the role of p38 Mitogen-activated protein kinase (MAPK) in imparting cisplatin resistance in head and neck squamous cell carcinoma (HNSCC) cells. Cisplatin 111-120 mitogen-activated protein kinase 14 Homo sapiens 54-90 33302041-2 2021 DESIGN: Laboratory generated cisplatin resistant HNSCC cells were treated with p38 inhibitor and were subjected to increasing dosage of cisplatin. Cisplatin 29-38 mitogen-activated protein kinase 14 Homo sapiens 79-82 33302041-3 2021 Western blot, immunohistochemistry and RT PCR analysis were performed to investigate expression level of p-p38 and Cancer stem cell (CSC) markers in cisplatin resistant HNSCC cells with or without p38 inhibitor. Cisplatin 149-158 mitogen-activated protein kinase 14 Homo sapiens 107-110 33302041-5 2021 In addition, alkaline comet assay and gamma-H2AX immunostaining were performed to evaluate the DNA damage response and repair abilities in cisplatin resistant HNSCC cells after p38 inhibition. Cisplatin 139-148 mitogen-activated protein kinase 14 Homo sapiens 177-180 33302041-6 2021 RESULTS: It was observed that following p38 inhibition, cisplatin resistant HNSCC cells exhibited significant reduction in expression of CSC markers, beta-catenin, reduced migration potential and sphere forming ability along with increased apoptotic index demonstrating there was increased sensitivity towards Cisplatin. Cisplatin 56-65 mitogen-activated protein kinase 14 Homo sapiens 40-43 33302041-6 2021 RESULTS: It was observed that following p38 inhibition, cisplatin resistant HNSCC cells exhibited significant reduction in expression of CSC markers, beta-catenin, reduced migration potential and sphere forming ability along with increased apoptotic index demonstrating there was increased sensitivity towards Cisplatin. Cisplatin 310-319 mitogen-activated protein kinase 14 Homo sapiens 40-43 33302041-8 2021 p38 inhibited cisplatin resistant HNSCC cells also exhibited increased DNA damage as measured by Comet assay and gamma-H2AX foci formation index. Cisplatin 14-23 mitogen-activated protein kinase 14 Homo sapiens 0-3 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 14 Homo sapiens 123-126 32764530-0 2020 Reelin Promotes Cisplatin Resistance by Induction of Epithelial-Mesenchymal Transition via p38/GSK3beta/Snail Signaling in Non-Small Cell Lung Cancer. Cisplatin 16-25 mitogen-activated protein kinase 14 Homo sapiens 91-94 32764530-10 2020 CONCLUSIONS These data indicated that Reelin induces DDP resistance of NSCLC by regulation of the p38/GSK3ss/Snail/EMT signaling pathway and provide evidence that Reelin suppression can be an effective strategy to suppress DDP resistance in NSCLC. Cisplatin 53-56 mitogen-activated protein kinase 14 Homo sapiens 98-101 30267330-11 2018 Furthermore, oleandrin alone or with cisplatin, activated the p38 MAPK/Elk-1 pathway. Cisplatin 37-46 mitogen-activated protein kinase 14 Homo sapiens 62-65 31991751-8 2020 Further, the results of adding inhibitors of these proteins indicates that the phosphorylation of p38 are the key mediators in AA-induced apoptosis in cisplatin-resistant human NPC cells. Cisplatin 151-160 mitogen-activated protein kinase 14 Homo sapiens 98-101 31991751-9 2020 This is the first study to demonstrate the AA-induced apoptotic pathway through the phosphorylation p38 in human cisplatin-resistant nasopharyngeal carcinoma. Cisplatin 113-122 mitogen-activated protein kinase 14 Homo sapiens 100-103 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 14 Homo sapiens 39-42 31706153-8 2019 In conclusion, we found that ADCY9, GSK3B, MAPK14, NCK1, NCOA2, PIK3CA, PIK3CB, PTK2, RHOB act as hub genes in the cisplatin-responsive regulatory network at the pro-apoptotic stages. Cisplatin 115-124 mitogen-activated protein kinase 14 Homo sapiens 43-49 31983124-10 2019 Furthermore, it was found that cetuximab + cisplatin group had a stronger phosphorylation ability of P38 in gastric cancer tissues than the cetuximab group (p<0.05). Cisplatin 43-52 mitogen-activated protein kinase 14 Homo sapiens 101-104 31983124-11 2019 CONCLUSIONS: Compared with cetuximab alone, cetuximab combined with cisplatin can significantly improve the clinical efficacy, reduce the tumor metastasis rate, enhance the immune function and improve the prognosis of gastric cancer patients, whose mechanism may be related to the activation of P38 in gastric cancer tissues. Cisplatin 68-77 mitogen-activated protein kinase 14 Homo sapiens 295-298 31205536-0 2019 CUEDC2 Contributes to Cisplatin-Based Chemotherapy Resistance in Ovarian Serious Carcinoma by Regulating p38 MAPK Signaling. Cisplatin 22-31 mitogen-activated protein kinase 14 Homo sapiens 105-108 31205536-8 2019 Our data suggest that CUEDC2 takes part in cisplatin-based chemotherapy resistance by regulating p38 MAPK signaling. Cisplatin 43-52 mitogen-activated protein kinase 14 Homo sapiens 97-100 30267330-0 2018 Oleandrin synergizes with cisplatin in human osteosarcoma cells by enhancing cell apoptosis through activation of the p38 MAPK signaling pathway. Cisplatin 26-35 mitogen-activated protein kinase 14 Homo sapiens 118-121 30944654-8 2019 Subsequent mechanistic analysis demonstrated that TNFAIP8 silencing promoted caspase-8/-3 activation and p38 phosphorylation in HeLa cells treated with cisplatin, whereas apoptosis regulator B-cell lymphoma-2 expression was inhibited with TNFAIP8-silenced HeLa cells following treatment with cisplatin. Cisplatin 152-161 mitogen-activated protein kinase 14 Homo sapiens 105-108 30267330-14 2018 CONCLUSIONS: The combination of oleandrin with cisplatin exerts a synergistic antitumor effect in osteosarcoma, which relates to the activation of the p38 MAPK pathway. Cisplatin 47-56 mitogen-activated protein kinase 14 Homo sapiens 151-154 29983416-10 2018 TRF2 silencing and p38 inhibition chemosensitize HNSCC cells to cisplatin. Cisplatin 64-73 mitogen-activated protein kinase 14 Homo sapiens 19-22 30344920-9 2018 Moreover, TIMP-1 upregulation and consequent inhibition of HUVEC migration by cisplatin was shown to be dependent on activation of p38 and p42/44 mitogen-activated protein kinases. Cisplatin 78-87 mitogen-activated protein kinase 14 Homo sapiens 131-134 29983416-0 2018 p38 MAPK pathway and its interaction with TRF2 in cisplatin induced chemotherapeutic response in head and neck cancer. Cisplatin 50-59 mitogen-activated protein kinase 14 Homo sapiens 0-3 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 14 Homo sapiens 67-70 29805654-0 2018 Cisplatin-induced non-canonical endocytosis of EGFR via p38 phosphorylation of the C-terminal region containing Ser-1015 in non-small cell lung cancer cells. Cisplatin 0-9 mitogen-activated protein kinase 14 Homo sapiens 56-59 29805654-5 2018 Cisplatin-induced p38 activation triggered the Ser-1015 phosphorylation of EGFR, with similar kinetics to previously reported Ser-1047 phosphorylation, in a tyrosine kinase-independent manner. Cisplatin 0-9 mitogen-activated protein kinase 14 Homo sapiens 18-21 28120035-7 2017 The pJNK/p38 pathway has been implicated in cisplatin cytotoxicity, and significant phosphorylation of pJNK was observed in the SKOV3 and ME180R and p38 in the SKOV3 knockdowns. Cisplatin 44-53 mitogen-activated protein kinase 14 Homo sapiens 9-12 29575240-8 2018 p38-inhibited cells showed significantly reduced expression of CSC markers, chemosensitivity toward cisplatin, reduced migration potential, and sphere-forming ability along with increased apoptotic population after treatment with increasing concentration of cisplatin. Cisplatin 100-109 mitogen-activated protein kinase 14 Homo sapiens 0-3 29575240-8 2018 p38-inhibited cells showed significantly reduced expression of CSC markers, chemosensitivity toward cisplatin, reduced migration potential, and sphere-forming ability along with increased apoptotic population after treatment with increasing concentration of cisplatin. Cisplatin 258-267 mitogen-activated protein kinase 14 Homo sapiens 0-3 29518977-4 2018 By combining statistical methods with available gene annotations and without a previously defined hypothesis HRas, MAPK14 (p38), CCL2, DOK1 and PTK2B were identified as genes possibly relevant for cisplatin resistance. Cisplatin 197-206 mitogen-activated protein kinase 14 Homo sapiens 115-121 29518977-4 2018 By combining statistical methods with available gene annotations and without a previously defined hypothesis HRas, MAPK14 (p38), CCL2, DOK1 and PTK2B were identified as genes possibly relevant for cisplatin resistance. Cisplatin 197-206 mitogen-activated protein kinase 14 Homo sapiens 123-126 29518977-6 2018 HRas, p38, CCL2, DOK1, PTK2B and JNK3 were integrated into a model of resistance-associated signalling alterations describing differential gene and protein expression between cisplatin-sensitive and -resistant cells in reaction to cisplatin exposure. Cisplatin 175-184 mitogen-activated protein kinase 14 Homo sapiens 6-9 28927101-13 2017 In addition, p38 inhibitor treatment significantly inhibited the mRNA and protein expression levels of ERCC1 in A549 cells, and enhanced the sensitivity of cells to cisplatin. Cisplatin 165-174 mitogen-activated protein kinase 14 Homo sapiens 13-16 27184254-11 2016 Upregulation of p38, a MAPK activated in response to cisplatin, was suppressed in HE4-overexpressing clones. Cisplatin 53-62 mitogen-activated protein kinase 14 Homo sapiens 16-19 27026405-0 2016 Curcumin downregulates p38 MAPK-dependent X-ray repair cross-complement group 1 (XRCC1) expression to enhance cisplatin-induced cytotoxicity in human lung cancer cells. Cisplatin 110-119 mitogen-activated protein kinase 14 Homo sapiens 23-26 27026405-4 2016 In this study, we characterize the role of curcumin in the cytotoxicity, p38 MAPK activation, and XRCC1 expression affected by cisplatin in NSCLC cells. Cisplatin 127-136 mitogen-activated protein kinase 14 Homo sapiens 73-76 27537399-0 2016 Id4 promotes cisplatin resistance in lung cancer through the p38 MAPK pathway. Cisplatin 13-22 mitogen-activated protein kinase 14 Homo sapiens 61-64 27537399-3 2016 Moreover, overexpression of Id4 in A549 cells results in cisplatin resistance and apoptosis inhibition, while increasing the IC50 for cisplatin through activation of phospho-p38 MAPK. Cisplatin 134-143 mitogen-activated protein kinase 14 Homo sapiens 174-177 27537399-5 2016 In addition, a p38 MAPK inhibitor (SB202190) could partly reverse both Id4-reduced apoptosis and Id4-induced cisplatin resistance. Cisplatin 109-118 mitogen-activated protein kinase 14 Homo sapiens 15-18 27537399-6 2016 These results suggest that Id4 inhibits cisplatin-induced apoptosis in human lung adenocarcinoma, partially through activation of the p38 MAPK pathway. Cisplatin 40-49 mitogen-activated protein kinase 14 Homo sapiens 134-137 27825085-0 2016 AKT2 inhibition of cisplatin-induced JNK/p38 and Bax activation by phosphorylation of ASK1. Cisplatin 19-28 mitogen-activated protein kinase 14 Homo sapiens 41-44 27026405-6 2016 Treatment with cisplatin alone increased XRCC1 mRNA and protein expression through p38 MAPK activation. Cisplatin 15-24 mitogen-activated protein kinase 14 Homo sapiens 83-86 27026405-7 2016 Moreover, SB2023580 (p38 inhibitor) decreased the XRCC1 mRNA and protein stability upon cisplatin treatment. Cisplatin 88-97 mitogen-activated protein kinase 14 Homo sapiens 21-24 27026405-8 2016 Knockdown of XRCC1 in NSCLC cells by transfection of XRCC1 siRNA or inactivation of p38 MAPK resulted in enhancing the cytotoxicity and cell growth inhibition induced by cisplatin. Cisplatin 170-179 mitogen-activated protein kinase 14 Homo sapiens 84-87 26586936-8 2015 When As4S4 was combined with chemotherapy drug cisplatin or COX2 inhibitor celecoxib, its inhibition of COX2, BCL2, and p38 expression was enhanced. Cisplatin 47-56 mitogen-activated protein kinase 14 Homo sapiens 120-123 26872057-9 2016 Knockdown of Hsp27 or p38 decreased cisplatin resistance and increased apoptosis in DRSPs. Cisplatin 36-45 mitogen-activated protein kinase 14 Homo sapiens 22-25 26872057-12 2016 SUMMARY: DRSPs were useful for investigating drug resistance and may provide a practical model for studying the crucial role of p-Hsp27 in the p38 MAPK-Hsp27 axis in CSC-mediated cisplatin resistance. Cisplatin 179-188 mitogen-activated protein kinase 14 Homo sapiens 143-146 27313779-12 2016 Inhibition of p38 activation decreased cisplatin"s induction of p53, but no difference in p38 activation by cisplatin was observed between 2D cultures and 3D cultures. Cisplatin 39-48 mitogen-activated protein kinase 14 Homo sapiens 14-17 26568478-0 2015 Tetrathiomolybdate mediates cisplatin-induced p38 signaling and EGFR degradation and enhances response to cisplatin therapy in gynecologic cancers. Cisplatin 28-37 mitogen-activated protein kinase 14 Homo sapiens 46-49 26568478-7 2015 TM suppressed cisplatin-induced activation of EGFR while potentiating activation of p38; the activation of p38 signaling appeared to promote cisplatin-induced EGFR degradation. Cisplatin 141-150 mitogen-activated protein kinase 14 Homo sapiens 107-110 26568478-10 2015 We furthermore provide evidence that TM may provide an additional benefit by potentiating p38 activation following cisplatin treatment, which may in turn promote receptor degradation by cisplatin. Cisplatin 115-124 mitogen-activated protein kinase 14 Homo sapiens 90-93 26586936-9 2015 As4S4 and cisplatin synergistically stimulated p53, phosphor-p38 (p-p38), and increased cleaved caspase 3 (c-caspase 3). Cisplatin 10-19 mitogen-activated protein kinase 14 Homo sapiens 61-64 26586936-9 2015 As4S4 and cisplatin synergistically stimulated p53, phosphor-p38 (p-p38), and increased cleaved caspase 3 (c-caspase 3). Cisplatin 10-19 mitogen-activated protein kinase 14 Homo sapiens 68-71 26310353-7 2015 We found that butein inhibited the activation of AKT, extracellular signal-regulated kinase (ERKs) and p38 kinases in the presence of cisplatin. Cisplatin 134-143 mitogen-activated protein kinase 14 Homo sapiens 103-106 26310353-9 2015 Of note, the inhibition of ERK or p38 MAPK by U0126 or SB203580, respectively, decreased the apoptosis induced by cisplatin; however, enhanced apoptotic effects were observed with the use of ERK/p38 MAPK inhibitor in combination with butein. Cisplatin 114-123 mitogen-activated protein kinase 14 Homo sapiens 34-37 26310353-0 2015 Butein sensitizes HeLa cells to cisplatin through the AKT and ERK/p38 MAPK pathways by targeting FoxO3a. Cisplatin 32-41 mitogen-activated protein kinase 14 Homo sapiens 66-69 26310353-9 2015 Of note, the inhibition of ERK or p38 MAPK by U0126 or SB203580, respectively, decreased the apoptosis induced by cisplatin; however, enhanced apoptotic effects were observed with the use of ERK/p38 MAPK inhibitor in combination with butein. Cisplatin 114-123 mitogen-activated protein kinase 14 Homo sapiens 195-198 26310353-10 2015 These data suggest that the AKT and ERK/p38 MAPK pathways are involved in the synergistic effects of butein and cisplatin. Cisplatin 112-121 mitogen-activated protein kinase 14 Homo sapiens 40-43 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 14 Homo sapiens 83-86 26066081-2 2015 We show that the p38 MAP kinase-dependent, EGFR tyrosine kinase (TK)-independent EGFR internalization induced by ultraviolet light C (UVC) or the cancer therapeutic cisplatin, is followed by diversion from the canonical endocytic pathway. Cisplatin 165-174 mitogen-activated protein kinase 14 Homo sapiens 17-20 26018318-7 2015 Overexpression of Twist in the two cell lines markedly increased GDF15 expression, cell invasion, matrix metalloproteinase-2 expression/activity and the half maximal inhibitory concentration (IC50) values of cisplatin, which was eradicated by GDF15 knockdown or the selective p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 (10 microM). Cisplatin 208-217 mitogen-activated protein kinase 14 Homo sapiens 276-312 26018318-10 2015 In conclusion, the present study, for the first time, to the best of our knowledge, demonstrated that Twist promotes PC cell invasion and cisplatin chemoresistance through inducing GDF15 expression via a p38 MAPK-dependent mechanism. Cisplatin 138-147 mitogen-activated protein kinase 14 Homo sapiens 204-207 26171149-8 2015 Cisplatin, the activator of p38 MAPK, also suppressed USP22 expression. Cisplatin 0-9 mitogen-activated protein kinase 14 Homo sapiens 28-31 25701783-5 2015 It is interesting that internalization mechanism of EGFR was switched from tyrosine kinase-dependent to p38-dependent fashions, which is involved in a survival pathway that counteracts cisplatin treatment. Cisplatin 185-194 mitogen-activated protein kinase 14 Homo sapiens 104-107 25894720-5 2015 RESULTS: Cisplatin treatment of a cervical cancer cell line resulted in ROS production with mitochondrial membrane depolarization and phosphorylation of JNK and p38. Cisplatin 9-18 mitogen-activated protein kinase 14 Homo sapiens 161-164 25894720-9 2015 Downregulation of dihydrodiol dehydrogenase in the cisplatin-resistant cervical and lung cancer cell lines resulted in increased drug sensitivity with detectable production of ROS and activation of the JNK/p38 pathways; however, downregulation of thioredoxin in the cervical cells had minimal effect. Cisplatin 51-60 mitogen-activated protein kinase 14 Homo sapiens 206-209 25765877-4 2015 Platinum derivatives, such as cisplatin and carboplatin, harm mainly peripheral nerves and dorsal root ganglia neurons, possibly because of progressive DNA-adduct accumulation and inhibition of DNA repair pathways (e.g., extracellular signal-regulated kinase 1/2, c-Jun N-terminal kinase/stress-activated protein kinase, and p38 mitogen-activated protein kinass), which finally mediate apoptosis. Cisplatin 30-39 mitogen-activated protein kinase 14 Homo sapiens 325-328 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 14 Homo sapiens 100-103 25118792-0 2014 Metformin combined with p38 MAPK inhibitor improves cisplatin sensitivity in cisplatin-resistant ovarian cancer. Cisplatin 52-61 mitogen-activated protein kinase 14 Homo sapiens 24-27 25118792-0 2014 Metformin combined with p38 MAPK inhibitor improves cisplatin sensitivity in cisplatin-resistant ovarian cancer. Cisplatin 77-86 mitogen-activated protein kinase 14 Homo sapiens 24-27 25118792-1 2014 The aim of the present study was to determine the effects of metformin, combined with a p38 mitogen-activated protein kinase (MAPK) inhibitor, on the sensitivity of cisplatin-resistant ovarian cancer to cisplatin. Cisplatin 165-174 mitogen-activated protein kinase 14 Homo sapiens 88-91 25118792-1 2014 The aim of the present study was to determine the effects of metformin, combined with a p38 mitogen-activated protein kinase (MAPK) inhibitor, on the sensitivity of cisplatin-resistant ovarian cancer to cisplatin. Cisplatin 203-212 mitogen-activated protein kinase 14 Homo sapiens 88-91 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 14 Homo sapiens 137-140 25118792-4 2014 The protein expression of P-p38 MAPK was significantly higher in cisplatin-resistant ovarian cancer, as compared with the primary ovarian cancer tissues. Cisplatin 65-74 mitogen-activated protein kinase 14 Homo sapiens 28-31 25118792-6 2014 In conclusion, the p38 MAPK signaling pathway may be associated with cisplatin-resistant ovarian cancer. Cisplatin 69-78 mitogen-activated protein kinase 14 Homo sapiens 19-22 25118792-7 2014 Metformin, combined with the p38 MAPK inhibitor, significantly increased the sensitivity of SKOV3/DDP cells to cisplatin treatment. Cisplatin 111-120 mitogen-activated protein kinase 14 Homo sapiens 29-32 25110412-3 2014 Resistance to cisplatin, irinotecan and 5-fluorouracil chemotherapy has been shown to involve mitogen-activated protein kinase (MAPK) signaling and recent studies identified p38alpha MAPK as a mediator of resistance to various agents in CRC patients. Cisplatin 14-23 mitogen-activated protein kinase 14 Homo sapiens 174-182 24988892-5 2014 Most importantly, lung cancer cells themselves upregulated IL-6 secretion by activating the p38/NF-kappaB pathway through treatment with cisplatin and camptothecin. Cisplatin 137-146 mitogen-activated protein kinase 14 Homo sapiens 92-95 24851838-3 2014 Exposure to cisplatin and UV radiation induced caspase-3-dependent apoptotic cell death, and p38 MAPK signaling de-regulation. Cisplatin 12-21 mitogen-activated protein kinase 14 Homo sapiens 93-96 24851838-8 2014 In addition, cisplatin-induced p38 sustained activation correlated perfectly with progressive reduction in DUSP2 expression. Cisplatin 13-22 mitogen-activated protein kinase 14 Homo sapiens 31-34 23933134-5 2013 Activation of the p38alpha MAPK signaling pathway has been suggested to be one of the main mechanisms by which cisplatin induces apoptosis. Cisplatin 111-120 mitogen-activated protein kinase 14 Homo sapiens 18-26 24796665-4 2014 ALA pretreatment significantly reduced apoptotic cell death of the inner and outer hair cells in cisplatin-treated organ of Corti explants and attenuated ototoxicity via marked inhibition of the increase in the expression of IL-1beta and IL-6, the phosphorylation of ERK and p38, the degradation of IkappaBalpha, the increase in intracellular levels of ROS, and the activation of caspase-3 in cisplatin-treated HEI-OC1 cells. Cisplatin 97-106 mitogen-activated protein kinase 14 Homo sapiens 275-278 23297007-7 2014 KR-22335 inhibited cisplatin-induced activation of JNK, p-38, caspase-3 and PARP in HEI-OC1 cells. Cisplatin 19-28 mitogen-activated protein kinase 14 Homo sapiens 56-60 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 14 Homo sapiens 14-17 24115572-3 2013 Here, we provide genetic and pharmacological evidence showing that p38 MAPK inhibition cooperates with the chemotherapeutic agent cisplatin to kill tumour cells. Cisplatin 130-139 mitogen-activated protein kinase 14 Homo sapiens 67-70 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 14 Homo sapiens 13-16 24115572-6 2013 Taken together, our results illustrate a new function of p38 MAPK that helps tumour cells to survive chemotherapeutic drug treatments, and reveal that the combination of p38 MAPK inhibitors with cisplatin can be potentially exploited for cancer therapy. Cisplatin 195-204 mitogen-activated protein kinase 14 Homo sapiens 57-60 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 14 Homo sapiens 42-50 24690178-5 2014 Cisplatin treatment of the knockdowns increased ROS levels significantly (as compared to the parental cells) and produced activation of the JNK/p38 pathways and activating transcription factor (ATF2). Cisplatin 0-9 mitogen-activated protein kinase 14 Homo sapiens 144-147 24215867-0 2014 Targeted therapy against chemoresistant colorectal cancers: Inhibition of p38alpha modulates the effect of cisplatin in vitro and in vivo through the tumor suppressor FoxO3A. Cisplatin 107-116 mitogen-activated protein kinase 14 Homo sapiens 74-82 24185104-0 2013 14-3-3sigma attenuates RhoGDI2-induced cisplatin resistance through activation of Erk and p38 in gastric cancer cells. Cisplatin 39-48 mitogen-activated protein kinase 14 Homo sapiens 90-93 24185104-6 2013 We also found that the phosphorylation levels of Erk and p38 kinases significantly decreased in RhoGDI2-overexpressing SNU-484 cells and recovered after 14-3-3sigma expression, and that decreased activities of these kinases were critical for RhoGDI2-induced cisplatin resistance. Cisplatin 258-267 mitogen-activated protein kinase 14 Homo sapiens 57-60 23933134-9 2013 An initial activation of the p38alpha MAPK signaling pathway was detected at early time points of cisplatin treatment, a response previously suggested to be part of the mechanism by which cisplatin induces apoptosis. Cisplatin 98-107 mitogen-activated protein kinase 14 Homo sapiens 29-37 23933134-9 2013 An initial activation of the p38alpha MAPK signaling pathway was detected at early time points of cisplatin treatment, a response previously suggested to be part of the mechanism by which cisplatin induces apoptosis. Cisplatin 188-197 mitogen-activated protein kinase 14 Homo sapiens 29-37 22027747-10 2011 In the cisplatin-treated cells, the expression of NLK was decreased, gradually through p38 signal pathway. Cisplatin 7-16 mitogen-activated protein kinase 14 Homo sapiens 87-90 23926438-6 2013 Furthermore, cordycepin or cisplatin induced caspase-8, caspase-9, caspase-3, and poly adenosine diphosphate-ribose polymerase protein cleavages, and stimulated c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, and p38 protein phosphorylations. Cisplatin 27-36 mitogen-activated protein kinase 14 Homo sapiens 231-234 23299493-6 2013 Cisplatin alone induced mRNA expression of excision repair cross complementation 1 (ERCC1) and thymidine phosphorylase (TP) through phosphorylation of ERK, p38 and PI3K/AKT pathways. Cisplatin 0-9 mitogen-activated protein kinase 14 Homo sapiens 156-159 22415779-2 2012 The authors investigated whether p38 MAPK activity contributed to the viability of cisplatin in lung cancer cell lines from never or light smokers and to ERCC1 mRNA expression. Cisplatin 83-92 mitogen-activated protein kinase 14 Homo sapiens 33-36 22415779-14 2012 Sensitization to cisplatin can be achieved by pharmacological inhibition of p38 MAPK signaling. Cisplatin 17-26 mitogen-activated protein kinase 14 Homo sapiens 76-79 23570372-0 2013 Phosphorylation of eIF2alpha suppresses cisplatin-induced A549 cell apoptosis via p38 inhibition. Cisplatin 40-49 mitogen-activated protein kinase 14 Homo sapiens 82-85 23570372-6 2013 Importantly, phospho-eIF2alpha inhibited cisplatin-induced A549 cells apoptosis, at least in part, by suppressing the p38 pathway. Cisplatin 41-50 mitogen-activated protein kinase 14 Homo sapiens 118-121 23019413-4 2012 The cisplatin-induced cellular stress response involved activation of p38alpha mitogen-activated protein kinase, whereas Titanocene Y-triggered signaling affected c-Jun N-terminal kinase. Cisplatin 4-13 mitogen-activated protein kinase 14 Homo sapiens 70-78 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 14 Homo sapiens 147-150 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 14 Homo sapiens 106-109 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 14 Homo sapiens 462-465 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 14 Homo sapiens 132-141 21898549-2 2012 Conversely, activation of p38 MAPK in tumor cells results in cancer cell cycle inhibition or apoptosis initiated by chemotherapeutic agents such as retinoids or cisplatin, and is therefore an attractive approach for experimental anti-tumor therapies. Cisplatin 161-170 mitogen-activated protein kinase 14 Homo sapiens 26-29 21320468-0 2011 Induction of ER stress protects gastric cancer cells against apoptosis induced by cisplatin and doxorubicin through activation of p38 MAPK. Cisplatin 82-91 mitogen-activated protein kinase 14 Homo sapiens 130-133 21993003-0 2011 Oxytocin inhibits NADPH oxidase and P38 MAPK in cisplatin-induced nephrotoxicity. Cisplatin 48-57 mitogen-activated protein kinase 14 Homo sapiens 36-39 21803700-5 2011 Our results show that DEX treatment inhibits cisplatin-induced cell apoptosis by up-regulation of cellular mitogen-activated protein kinase phosphatase-1 (MKP-1) and subsequent deactivation of p38 protein kinase. Cisplatin 45-54 mitogen-activated protein kinase 14 Homo sapiens 193-196 21320468-4 2011 Inhibition of p38 activity abrogated the effects of ER stress-induced resistance to apoptosis induced by cisplatin- and doxorubicin treatment. Cisplatin 105-114 mitogen-activated protein kinase 14 Homo sapiens 14-17 21320468-5 2011 Thus, ER-stress response in gastric cancer cells causes resistance to cisplatin- and doxorubicin-induced apoptosis, and ER-stress induced chemo-resistance can be overcome by blocking p38 activity. Cisplatin 70-79 mitogen-activated protein kinase 14 Homo sapiens 183-186 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 14 Homo sapiens 108-111 21165580-0 2011 Tanshinone IIA acts via p38 MAPK to induce apoptosis and the down-regulation of ERCC1 and lung-resistance protein in cisplatin-resistant ovarian cancer cells. Cisplatin 117-126 mitogen-activated protein kinase 14 Homo sapiens 24-27 22164285-0 2011 Balance between MKK6 and MKK3 mediates p38 MAPK associated resistance to cisplatin in NSCLC. Cisplatin 73-82 mitogen-activated protein kinase 14 Homo sapiens 39-42 22164285-1 2011 The p38 MAPK signaling pathway has been proposed as a critical mediator of the therapeutic effect of several antitumor agents, including cisplatin. Cisplatin 137-146 mitogen-activated protein kinase 14 Homo sapiens 4-7 22164285-2 2011 Here, we found that sensitivity to cisplatin, in a system of 7 non-small cell lung carcinoma derived cell lines, correlated with high levels of MKK6 and marked activation of p38 MAPK. Cisplatin 35-44 mitogen-activated protein kinase 14 Homo sapiens 174-177 22164285-5 2011 Interestingly, MKK3 knockdown significantly decreased p38 phosphorylation upon cisplatin exposure and consequently reduced the response to the drug. Cisplatin 79-88 mitogen-activated protein kinase 14 Homo sapiens 54-57 22164285-10 2011 Altogether, our work provides evidence that MKK3 is the major determinant of p38 MAPK activation in response to cisplatin and, hence, the resistance associated with this MAPK. Cisplatin 112-121 mitogen-activated protein kinase 14 Homo sapiens 77-80 19435873-0 2009 Inhibition of the met receptor tyrosine kinase signaling enhances the chemosensitivity of glioma cell lines to CDDP through activation of p38 MAPK pathway. Cisplatin 111-115 mitogen-activated protein kinase 14 Homo sapiens 138-141 19435873-6 2009 Therefore, p38 MAPK activation was one of the major causes for the increased chemosensitivity to CDDP induced by Met inactivation. Cisplatin 97-101 mitogen-activated protein kinase 14 Homo sapiens 11-14 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 14 Homo sapiens 206-209 17893873-0 2008 c-Abl activates p38 MAPK independently of its tyrosine kinase activity: Implications in cisplatin-based therapy. Cisplatin 88-97 mitogen-activated protein kinase 14 Homo sapiens 16-19 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 14 Homo sapiens 124-132 17893873-1 2008 Activation of p38 MAPK is a critical requisite for the therapeutics activity of the antitumor agent cisplatin. Cisplatin 100-109 mitogen-activated protein kinase 14 Homo sapiens 14-17 17893873-2 2008 In this sense, a growing body of evidences supports the role of c-Abl as a major determinant of p38 MAPK activation, especially in response to genotoxic stress when triggered by cisplatin. Cisplatin 178-187 mitogen-activated protein kinase 14 Homo sapiens 96-99 17893873-3 2008 Here, we demonstrate that p38 MAPK activation in response to cisplatin does not require the tyrosine kinase activity of c-Abl. Cisplatin 61-70 mitogen-activated protein kinase 14 Homo sapiens 26-29 17369856-5 2007 Cisplatin"s effects on TIMP-1 expression and invasion were associated with phosphorylations of p38 and p42/44 mitogen-activated protein kinases and were abrogated by specific inhibitors of both pathways. Cisplatin 0-9 mitogen-activated protein kinase 14 Homo sapiens 95-98 17505786-0 2007 Apoptosis by cisplatin requires p53 mediated p38alpha MAPK activation through ROS generation. Cisplatin 13-22 mitogen-activated protein kinase 14 Homo sapiens 45-53 17505786-3 2007 Using the HCT116 colon carcinoma derived cell line we have established that the apoptotic activity of cisplatin requires the onset of a p53-mediated p38alpha MAPK pathway through generation of reactive oxygen species (ROS). Cisplatin 102-111 mitogen-activated protein kinase 14 Homo sapiens 149-157 17505786-6 2007 In addition, we have identified p38alpha as the isoform necessary for cisplatin-induced apoptosis, upon activation by p53-mediated ROS production. Cisplatin 70-79 mitogen-activated protein kinase 14 Homo sapiens 32-40 17505786-8 2007 We conclude that the p53/ROS/p38alpha MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38alpha/p53 positive feedback loop strongly enhances the initial p53 activation. Cisplatin 68-77 mitogen-activated protein kinase 14 Homo sapiens 29-37 17505786-8 2007 We conclude that the p53/ROS/p38alpha MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38alpha/p53 positive feedback loop strongly enhances the initial p53 activation. Cisplatin 68-77 mitogen-activated protein kinase 14 Homo sapiens 132-140 16785992-0 2006 Cisplatin induces PKB/Akt activation and p38(MAPK) phosphorylation of the EGF receptor. Cisplatin 0-9 mitogen-activated protein kinase 14 Homo sapiens 41-44 17504983-2 2007 It is attempted to know how Hsp27 endues cell with cisplatin resistance by interfering with upstream of both apoptosis signal-regulating kinase 1 (ASK1)/p38 mitogen-activated protein kinase-activated apoptotic signaling and serine/threonine kinase Akt-dependent survival signaling. Cisplatin 51-60 mitogen-activated protein kinase 14 Homo sapiens 153-156 17504983-4 2007 The cisplatin-induced apoptosis and activation of ASK1, p38, and Akt were compared in control cells, cells overexpressing Hsp27, and cells with their endogenous Hsp27 knocked down. Cisplatin 4-13 mitogen-activated protein kinase 14 Homo sapiens 56-59 17504983-6 2007 The p38 inhibitors obviously decreased whereas Akt inhibitors markedly increased the apoptotic fraction in cisplatin-treated cells. Cisplatin 107-116 mitogen-activated protein kinase 14 Homo sapiens 4-7 17504983-10 2007 CONCLUSIONS: Hsp27 endues cells with cisplatin resistance via depression of the drug-induced ASK1/p38 activation and enhancement of the drug-induced Akt activation. Cisplatin 37-46 mitogen-activated protein kinase 14 Homo sapiens 98-101 17699106-0 2007 (Dihydro)ceramide synthase 1 regulated sensitivity to cisplatin is associated with the activation of p38 mitogen-activated protein kinase and is abrogated by sphingosine kinase 1. Cisplatin 54-63 mitogen-activated protein kinase 14 Homo sapiens 101-137 16785992-4 2006 While investigating the EGFR-dependent PKB/Akt activation in MDA-MB-468 cells, we found that the EGFR receptor undergoes a gel mobility shift upon Cisplatin treatment, which is mediated by p38(MAPK). Cisplatin 147-156 mitogen-activated protein kinase 14 Homo sapiens 189-192 16785992-6 2006 We found that Cisplatin induces EGFR internalization, which is mediated by p38(MAPK-)dependent phosphorylation of the receptor on threonine 669. Cisplatin 14-23 mitogen-activated protein kinase 14 Homo sapiens 75-78 15886300-8 2005 Studies using inhibitors to specific mitogen-activated protein kinases (MAPK) show that the increased cisplatin sensitivity in the hSPL-overexpressing cells is mediated by p38 and to a lesser extent by c-Jun NH2-terminal kinase MAPKs. Cisplatin 102-111 mitogen-activated protein kinase 14 Homo sapiens 172-175 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 14 Homo sapiens 89-92 16052670-6 2005 RESULTS: (1) Both cisplatin and DTT induced apoptosis in the esophageal cancer cell line Eca109 as shown by DNA ladder formation; (2) As detected by antibodies specific for the phosphorylated P38 protein (p-P38), both cisplatin and DTT treatments activated the stress-activated enzyme, MAP kinase P38. Cisplatin 218-227 mitogen-activated protein kinase 14 Homo sapiens 192-195 16052670-8 2005 DTT treatment, but not cisplatin treatment, induces nuclear localization of p-P38; (3) As measured by flow cytometry, inhibition of P38 activity by SB203580 blocks DTT- and cisplatin-induced apoptosis. Cisplatin 173-182 mitogen-activated protein kinase 14 Homo sapiens 132-135 16052670-10 2005 Addition of the SB compound during the incubation reduced the apoptotic rate to about 7.6% for all the treatment groups, suggesting that P38 activation is essential for cisplatin- and DTT-induced apoptosis in Eca109 cells. Cisplatin 169-178 mitogen-activated protein kinase 14 Homo sapiens 137-140 16052670-11 2005 CONCLUSION: (1) Both DTT and cisplatin were able to induce apoptosis in esophageal cancer cell line Eca109; (2) P38 MAP kinase is essential for DTT- and cisplatin-induced apoptosis in Eca109 cells; (3) P38 activation may be the common signaling component relaying the multiple upstream signaling events to the downstream cell death program. Cisplatin 29-38 mitogen-activated protein kinase 14 Homo sapiens 112-126 16052670-11 2005 CONCLUSION: (1) Both DTT and cisplatin were able to induce apoptosis in esophageal cancer cell line Eca109; (2) P38 MAP kinase is essential for DTT- and cisplatin-induced apoptosis in Eca109 cells; (3) P38 activation may be the common signaling component relaying the multiple upstream signaling events to the downstream cell death program. Cisplatin 29-38 mitogen-activated protein kinase 14 Homo sapiens 112-115 16052670-11 2005 CONCLUSION: (1) Both DTT and cisplatin were able to induce apoptosis in esophageal cancer cell line Eca109; (2) P38 MAP kinase is essential for DTT- and cisplatin-induced apoptosis in Eca109 cells; (3) P38 activation may be the common signaling component relaying the multiple upstream signaling events to the downstream cell death program. Cisplatin 153-162 mitogen-activated protein kinase 14 Homo sapiens 112-126 16052670-11 2005 CONCLUSION: (1) Both DTT and cisplatin were able to induce apoptosis in esophageal cancer cell line Eca109; (2) P38 MAP kinase is essential for DTT- and cisplatin-induced apoptosis in Eca109 cells; (3) P38 activation may be the common signaling component relaying the multiple upstream signaling events to the downstream cell death program. Cisplatin 153-162 mitogen-activated protein kinase 14 Homo sapiens 112-115 16387351-0 2006 Acquisition of chemoresistance following discontinuous exposures to cisplatin is associated in ovarian carcinoma cells with progressive alteration of FAK, ERK and p38 activation in response to treatment. Cisplatin 68-77 mitogen-activated protein kinase 14 Homo sapiens 163-166 16387351-7 2006 The simultaneous study of activation pattern of key proteins of different signaling pathways revealed that cisplatin induced both activation of ERK and p38 and inhibition of P-FAK in the sensitive cells, whereas it progressively failed to elicit such a response in the resistant variants. Cisplatin 107-116 mitogen-activated protein kinase 14 Homo sapiens 152-155 16331246-0 2006 Protection of glioblastoma cells from cisplatin cytotoxicity via protein kinase Ciota-mediated attenuation of p38 MAP kinase signaling. Cisplatin 38-47 mitogen-activated protein kinase 14 Homo sapiens 110-113 16331246-9 2006 The expression of both GMFbeta mRNA and protein increased upon PKCiota depletion, and this was accompanied by an increase in cisplatin-activated p38 MAP kinase signaling. Cisplatin 125-134 mitogen-activated protein kinase 14 Homo sapiens 145-148 16331246-10 2006 Transient overexpression of GMFbeta increased cisplatin-activated p38 MAP kinase signaling and also sensitised cells to cisplatin cytotoxicity. Cisplatin 46-55 mitogen-activated protein kinase 14 Homo sapiens 66-69 16331246-11 2006 The increase in cisplatin cytotoxicity seen with PKCiota depletion was blocked by the p38 MAP kinase inhibitor SKF86002. Cisplatin 16-25 mitogen-activated protein kinase 14 Homo sapiens 86-89 16331246-12 2006 These data show that PKCiota can confer partial resistance to cisplatin in glioblastoma cells by suppressing GMFbeta-mediated enhancement of p38 MAP kinase signaling. Cisplatin 62-71 mitogen-activated protein kinase 14 Homo sapiens 141-144 16052670-0 2005 Role of stress-activated MAP kinase P38 in cisplatin- and DTT-induced apoptosis of the esophageal carcinoma cell line Eca109. Cisplatin 43-52 mitogen-activated protein kinase 14 Homo sapiens 36-39 16052670-1 2005 AIM: To study the role of P38 kinase in esophageal cancer cell apoptosis induced by genotoxin, cisplatin and the unfolded protein response (UPR) inducer, dithiothreitol (DTT). Cisplatin 95-104 mitogen-activated protein kinase 14 Homo sapiens 26-29 16052670-6 2005 RESULTS: (1) Both cisplatin and DTT induced apoptosis in the esophageal cancer cell line Eca109 as shown by DNA ladder formation; (2) As detected by antibodies specific for the phosphorylated P38 protein (p-P38), both cisplatin and DTT treatments activated the stress-activated enzyme, MAP kinase P38. Cisplatin 18-27 mitogen-activated protein kinase 14 Homo sapiens 192-195 16052670-6 2005 RESULTS: (1) Both cisplatin and DTT induced apoptosis in the esophageal cancer cell line Eca109 as shown by DNA ladder formation; (2) As detected by antibodies specific for the phosphorylated P38 protein (p-P38), both cisplatin and DTT treatments activated the stress-activated enzyme, MAP kinase P38. Cisplatin 18-27 mitogen-activated protein kinase 14 Homo sapiens 207-210 16052670-6 2005 RESULTS: (1) Both cisplatin and DTT induced apoptosis in the esophageal cancer cell line Eca109 as shown by DNA ladder formation; (2) As detected by antibodies specific for the phosphorylated P38 protein (p-P38), both cisplatin and DTT treatments activated the stress-activated enzyme, MAP kinase P38. Cisplatin 18-27 mitogen-activated protein kinase 14 Homo sapiens 207-210 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 14 Homo sapiens 34-37 15496615-8 2005 Specific kinase inhibitors demonstrated that cisplatin induced apoptosis through the p38 mitogen-activated protein kinase (MAPK) pathway, not the extracellular signal-regulated kinase MAPK pathway. Cisplatin 45-54 mitogen-activated protein kinase 14 Homo sapiens 85-121 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 14 Homo sapiens 103-106 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 14 Homo sapiens 28-31 15102355-1 2004 Recent studies show that activation of p38 mitogen-activated protein kinase (MAPK) results in cancer cell apoptosis initiated by retinoids, cisplatin and other chemotherapeutic agents. Cisplatin 140-149 mitogen-activated protein kinase 14 Homo sapiens 39-75 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 14 Homo sapiens 155-158 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 14 Homo sapiens 28-31 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 14 Homo sapiens 155-158 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 14 Homo sapiens 122-125 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 14 Homo sapiens 122-125 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 14 Homo sapiens 100-103 15010460-5 2004 We discovered that specific phosphorylation of histone H3 at Ser-10, mediated by the p38 MAPK pathway, is induced in response to cisplatin treatment. Cisplatin 129-138 mitogen-activated protein kinase 14 Homo sapiens 85-88 34216662-6 2021 Also, growing the cells in the scaffold sensitize the hepatocytes to the anti-tumor effect of cisplatin, by a mechanism involving the activation of ERK/p38alpha-MAPK and dysregulation of NF-kB/STAT3/Bcl-2 pathways. Cisplatin 94-103 mitogen-activated protein kinase 14 Homo sapiens 152-160 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 14 Homo sapiens 328-331 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 14 Homo sapiens 108-111 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 14 Homo sapiens 74-77 12821934-0 2003 Role of the p38 MAPK pathway in cisplatin-based therapy. Cisplatin 32-41 mitogen-activated protein kinase 14 Homo sapiens 12-15 12821934-2 2003 To determine whether the activation of p38 MAPK could be specific to cancer therapy, we investigated the activation of p38 MAPK in response to several chemotherapeutic agents, such as cisplatin, doxorubicin and taxol in several human cell lines. Cisplatin 184-193 mitogen-activated protein kinase 14 Homo sapiens 39-42 12821934-2 2003 To determine whether the activation of p38 MAPK could be specific to cancer therapy, we investigated the activation of p38 MAPK in response to several chemotherapeutic agents, such as cisplatin, doxorubicin and taxol in several human cell lines. Cisplatin 184-193 mitogen-activated protein kinase 14 Homo sapiens 119-122 12821934-4 2003 Only cisplatin was able to activate p38 MAPK in all the cell lines tested. Cisplatin 5-14 mitogen-activated protein kinase 14 Homo sapiens 36-39 12821934-6 2003 The kinetics of this activation is a key event in the biological role of p38 MAPK in response to cisplatin, as we conclude from the differences observed after treatment with transplatin and cisplatin. Cisplatin 97-106 mitogen-activated protein kinase 14 Homo sapiens 73-76 12821934-6 2003 The kinetics of this activation is a key event in the biological role of p38 MAPK in response to cisplatin, as we conclude from the differences observed after treatment with transplatin and cisplatin. Cisplatin 190-199 mitogen-activated protein kinase 14 Homo sapiens 73-76 12821934-8 2003 Although the isoforms alpha/beta are mainly activated, we also demonstrated that other members of the p38 MAPK family were susceptible to activation by cisplatin when they were overexpressed in 293 T. Finally, pretreatment with specific inhibitors (SB 203580 and SKF 86002) induces a resistant phenotype in response to cisplatin. Cisplatin 152-161 mitogen-activated protein kinase 14 Homo sapiens 102-105 12821934-8 2003 Although the isoforms alpha/beta are mainly activated, we also demonstrated that other members of the p38 MAPK family were susceptible to activation by cisplatin when they were overexpressed in 293 T. Finally, pretreatment with specific inhibitors (SB 203580 and SKF 86002) induces a resistant phenotype in response to cisplatin. Cisplatin 319-328 mitogen-activated protein kinase 14 Homo sapiens 102-105 12821934-10 2003 Therefore, we conclude that the p38 MAPK pathway is a specific target for cisplatin-based therapy with clinical implications. Cisplatin 74-83 mitogen-activated protein kinase 14 Homo sapiens 32-35 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 14 Homo sapiens 64-67 12824923-9 2003 By immunoblotting, these proteins were identified as c-Jun N-terminal kinase (JNK) 2 and p38 mitogen-activated protein kinase (MAPK) delta, respectively, both of which are believed to be involved in apoptosis induction by CDDP. Cisplatin 222-226 mitogen-activated protein kinase 14 Homo sapiens 89-125 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 14 Homo sapiens 41-44 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 14 Homo sapiens 28-31 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 14 Homo sapiens 62-65 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 14 Homo sapiens 12-15 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 14 Homo sapiens 241-244 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 14 Homo sapiens 12-15 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 14 Homo sapiens 241-244 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 14 Homo sapiens 12-15 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 14 Homo sapiens 241-244 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 14 Homo sapiens 64-67 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 14 Homo sapiens 31-67 11095975-2 2000 Here we show that another p38 family member is also activated in response to cisplatin exposure in human melanoma cells. Cisplatin 77-86 mitogen-activated protein kinase 14 Homo sapiens 26-29 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 14 Homo sapiens 154-157 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 14 Homo sapiens 295-298 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 14 Homo sapiens 295-298 8798604-3 1996 Here we show that diverse classes of DNA-damaging agents such as cisplatinum, 1-beta-D-arabinofuranosylcytosine, UV light, ionizing radiation, and methyl methanesulfonate activate p38 MAP kinase. Cisplatin 65-76 mitogen-activated protein kinase 14 Homo sapiens 180-183 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 14 Homo sapiens 73-76 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 14 Homo sapiens 103-106