PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31424641-10 2019 Curzerenone induced cell death in gemcitabine-resistant lung cancer cells by activating p38 MAPK/ERK signalling pathway while NF-kB pathway was inhibited in a dose-dependent manner. gemcitabine 34-45 mitogen-activated protein kinase 1 Homo sapiens 97-100 30866697-8 2019 Dasatinib with paclitaxel or gemcitabine combination also inhibits p-SRC, p-STAT3, p-AKT, and/or p-ERK in these pancreatic cancer cells. gemcitabine 29-40 mitogen-activated protein kinase 1 Homo sapiens 99-102 29848706-0 2018 Fisetin Enhances the Cytotoxicity of Gemcitabine by Down-regulating ERK-MYC in MiaPaca-2 Human Pancreatic Cancer Cells. gemcitabine 37-48 mitogen-activated protein kinase 1 Homo sapiens 68-71 30577630-8 2018 Mechanistically, pretreatment with ERK1/2 or p38 inhibitors significantly abrogated gemcitabine-mediated MVP release, indicating the involvement of mitogen-activated protein kinase (MAPK) pathway in PAF-R-dependent gemcitabine-mediated MVP release. gemcitabine 84-95 mitogen-activated protein kinase 1 Homo sapiens 45-48 30662800-5 2018 In addition, CUDC-101 enhanced gemcitabine-induced apoptosis via inhibited PI3K/Akt/mTOR and Erk pathway activation, as indicated by the phosphorylation status of Akt, 4EBP1, S6 and Erk. gemcitabine 31-42 mitogen-activated protein kinase 1 Homo sapiens 93-96 30662800-5 2018 In addition, CUDC-101 enhanced gemcitabine-induced apoptosis via inhibited PI3K/Akt/mTOR and Erk pathway activation, as indicated by the phosphorylation status of Akt, 4EBP1, S6 and Erk. gemcitabine 31-42 mitogen-activated protein kinase 1 Homo sapiens 182-185 29848706-7 2018 CONCLUSION: Fisetin sensitized human pancreatic cancer cells to gemcitabine-induced cytotoxicity through inhibition of ERK-MYC signaling. gemcitabine 64-75 mitogen-activated protein kinase 1 Homo sapiens 119-122 29960845-9 2018 Surprisingly, gemcitabine combined with SCH772984 (a suppressor of ERK pathway) could reverse the drug resistance resulted from overexpression of TUG1. gemcitabine 14-25 mitogen-activated protein kinase 1 Homo sapiens 67-70 28720574-7 2017 Treatment with gemcitabine caused undesirable activation of ERK1/2 in PDAC cells, but cotreatment with the FBP1-derived small peptide inhibitor FBP1 E4 overcame gemcitabine-induced ERK activation, thereby increasing the anticancer efficacy of gemcitabine in PDAC. gemcitabine 15-26 mitogen-activated protein kinase 1 Homo sapiens 60-63 29749405-0 2018 Natural compound Oblongifolin C confers gemcitabine resistance in pancreatic cancer by downregulating Src/MAPK/ERK pathways. gemcitabine 40-51 mitogen-activated protein kinase 1 Homo sapiens 111-114 29069735-0 2017 HMGB1-mediated autophagy attenuates gemcitabine-induced apoptosis in bladder cancer cells involving JNK and ERK activation. gemcitabine 36-47 mitogen-activated protein kinase 1 Homo sapiens 108-111 28797284-10 2017 In particular, gambogic acid reduced the expression of the ribonucleotide reductase subunit-M2 (RRM2) protein and mRNA, a trend that correlated with resistance to gemcitabine through inhibition of the extracellular signal-regulated kinase (ERK)/E2F1 signaling pathway. gemcitabine 163-174 mitogen-activated protein kinase 1 Homo sapiens 201-238 28797284-13 2017 CONCLUSIONS: These results demonstrate that gambogic acid sensitizes pancreatic cancer cells to gemcitabine in vitro and in vivo by inhibiting the activation of the ERK/E2F1/RRM2 signaling pathway. gemcitabine 96-107 mitogen-activated protein kinase 1 Homo sapiens 165-168 29069735-8 2017 Interestingly, suppressing HMGB1 expression attenuated gemcitabine-induced ERK and JNK activation and Bcl-2 phosphorylation. gemcitabine 55-66 mitogen-activated protein kinase 1 Homo sapiens 75-78 29069735-7 2017 Further, gemcitabine activated c-Jun N-terminal kinase (JNK) and extracellular regulated protein kinase (ERK) and Bcl-2 phosphorylation, and blocking ERK and JNK inhibited autophagy and increased apoptosis in gemcitabine-treated cells. gemcitabine 9-20 mitogen-activated protein kinase 1 Homo sapiens 65-103 29069735-9 2017 Thus, our results suggest that while gemcitabine kills bladder cancer cells through apoptosis, a cytoprotective autophagy is also induced involving HMGB1-mediated JNK and ERK to counteract the cytotoxicity of gemcitabine, and intervention targeting this pathway may improve the anticancer efficacy of gemcitabine against bladder cancer. gemcitabine 209-220 mitogen-activated protein kinase 1 Homo sapiens 171-174 29069735-7 2017 Further, gemcitabine activated c-Jun N-terminal kinase (JNK) and extracellular regulated protein kinase (ERK) and Bcl-2 phosphorylation, and blocking ERK and JNK inhibited autophagy and increased apoptosis in gemcitabine-treated cells. gemcitabine 9-20 mitogen-activated protein kinase 1 Homo sapiens 105-108 29069735-9 2017 Thus, our results suggest that while gemcitabine kills bladder cancer cells through apoptosis, a cytoprotective autophagy is also induced involving HMGB1-mediated JNK and ERK to counteract the cytotoxicity of gemcitabine, and intervention targeting this pathway may improve the anticancer efficacy of gemcitabine against bladder cancer. gemcitabine 209-220 mitogen-activated protein kinase 1 Homo sapiens 171-174 23091117-2 2013 As gemcitabine is active in S-phase, and the extracellular signal-regulated kinase (ERK) pathway has a major role driving cell-cycle progression, concurrent use of a MEK inhibitor could potentially antagonize the effect of gemcitabine. gemcitabine 223-234 mitogen-activated protein kinase 1 Homo sapiens 45-82 27384485-0 2016 Inhibition of ERalpha/ERK/P62 cascades induces "autophagic switch" in the estrogen receptor-positive breast cancer cells exposed to gemcitabine. gemcitabine 132-143 mitogen-activated protein kinase 1 Homo sapiens 22-25 27384485-5 2016 Gemcitabine treatment leads to the activation of ERalpha-ERK-P62 signal pathway in MCF-7 cells which may augment the autophagic degradation, thus results in the excessive activation of autophagy and irreversible autophagic cell death eventually. gemcitabine 0-11 mitogen-activated protein kinase 1 Homo sapiens 57-60 25946136-6 2015 Combination of let-7b mimic with paclitaxel or gemcitabine diminished MEK/ERK and PI3K/AKT signaling concurrently, triggered the onset of apoptosis, and reverted the epithelial-mesenchymal transition in KRAS mutant tumor cells. gemcitabine 47-58 mitogen-activated protein kinase 1 Homo sapiens 74-77 23320839-11 2013 Treatment of gemcitabine or doxorubicin activated phosphorylated ERK and induced the upregulation of MRP1 and MRP3. gemcitabine 13-24 mitogen-activated protein kinase 1 Homo sapiens 65-68 23091117-2 2013 As gemcitabine is active in S-phase, and the extracellular signal-regulated kinase (ERK) pathway has a major role driving cell-cycle progression, concurrent use of a MEK inhibitor could potentially antagonize the effect of gemcitabine. gemcitabine 223-234 mitogen-activated protein kinase 1 Homo sapiens 84-87 21529991-11 2011 CONCLUSIONS: These data demonstrate that sorafenib and gemcitabine synergistically interact against NSCLC cells, through suppression of Akt, c-Kit and ERK phosphorylation, induction of apoptosis and modulation of dCK, RRM1, RRM2 and RKIP gene expression. gemcitabine 55-66 mitogen-activated protein kinase 1 Homo sapiens 151-154 22110196-15 2011 These results provide evidence that ERK activity underlies sensitivity to gemcitabine and that addition of an agent that reduces this activity, such as lenalidomide, enhances gemcitabine efficacy. gemcitabine 74-85 mitogen-activated protein kinase 1 Homo sapiens 36-39 20726858-10 2010 Combined treatment with an inhibitor for amphiregulin and gemcitabine, paclitaxel, or cisplatin induced synergistic antitumor effects, accompanied by the suppression of Akt and ERK activation. gemcitabine 58-69 mitogen-activated protein kinase 1 Homo sapiens 177-180 21277645-0 2011 ERK phosphorylation predicts synergism between gemcitabine and the epidermal growth factor receptor inhibitor AG1478. gemcitabine 47-58 mitogen-activated protein kinase 1 Homo sapiens 0-3 21277645-10 2011 Furthermore, ERK phosphorylation was increased by gemcitabine and its suppression by AG1478 was related to antagonism particularly in H322. gemcitabine 50-61 mitogen-activated protein kinase 1 Homo sapiens 13-16 21277645-13 2011 CONCLUSION: Our findings are consistent with a model in which ERK phosphorylation favors synergy and the outcome depends on the balance between gemcitabine-induced and AG1478-inhibited ERK phosphorylation. gemcitabine 144-155 mitogen-activated protein kinase 1 Homo sapiens 62-65 20726858-8 2010 Treatment with gemcitabine, which reduced the cell viability and augmented the cell apoptotic rate, activated and subsequently attenuated ERK and EGFR signals. gemcitabine 15-26 mitogen-activated protein kinase 1 Homo sapiens 138-141 15476743-0 2004 Extracellular signal-regulated kinase activation and Bcl-2 downregulation mediate apoptosis after gemcitabine treatment partly via a p53-independent pathway. gemcitabine 98-109 mitogen-activated protein kinase 1 Homo sapiens 0-37 17054996-5 2006 Inhibition of the ERK pathway by PD98059 sensitized cells to 5-fluorouracil (5-FU), whereas cells became more resistant to Adriamycin (ADM; Meiji Seika, Tokyo, Japan) and gemcitabine (GEM). gemcitabine 171-182 mitogen-activated protein kinase 1 Homo sapiens 18-21 16818479-9 2006 However, all responders to gemcitabine exhibited (+) p-Erk expression [RR 30.6% for p-Erk (+) versus 0% for p-Erk (-), P = 0.01]. gemcitabine 27-38 mitogen-activated protein kinase 1 Homo sapiens 55-58 16818479-9 2006 However, all responders to gemcitabine exhibited (+) p-Erk expression [RR 30.6% for p-Erk (+) versus 0% for p-Erk (-), P = 0.01]. gemcitabine 27-38 mitogen-activated protein kinase 1 Homo sapiens 86-89 15476743-5 2004 Moreover, phosphorylated activation of extracellular signal-regulated kinase (ERK) was observed upon gemcitabine treatment. gemcitabine 101-112 mitogen-activated protein kinase 1 Homo sapiens 39-76 15476743-5 2004 Moreover, phosphorylated activation of extracellular signal-regulated kinase (ERK) was observed upon gemcitabine treatment. gemcitabine 101-112 mitogen-activated protein kinase 1 Homo sapiens 78-81 15476743-6 2004 Genetical or pharmacological inhibition of ERK activation markedly blocked gemcitabine-induced cell death. gemcitabine 75-86 mitogen-activated protein kinase 1 Homo sapiens 43-46 15476743-8 2004 Taken together, our observations indicate that ERK activation and Akt inactivation mediated gemcitabine-induced apoptosis independently of p53 in human NSCLC H1299 cells. gemcitabine 92-103 mitogen-activated protein kinase 1 Homo sapiens 47-50 11278435-5 2001 Gemcitabine treatment resulted in a moderate increase in the percentage of apoptotic cells that was accompanied by activation of p38 and MAPK (ERK1/2). gemcitabine 0-11 mitogen-activated protein kinase 1 Homo sapiens 129-132 15073105-10 2004 CONCLUSIONS: These data demonstrate that hypoxia can induce resistance of pancreatic cancer cells to gemcitabine mainly through the PI3K/Akt/NF-kappa B pathways and partially through the MAPK(Erk) signaling pathway. gemcitabine 101-112 mitogen-activated protein kinase 1 Homo sapiens 192-195 11278435-13 2001 These data indicate that suppression of Akt and MAPK in the presence of activated p38 results in cell death and a possible mechanism for the enhanced apoptosis produced by the combination of CI-1033 and gemcitabine in MDA-MB-453 cells. gemcitabine 203-214 mitogen-activated protein kinase 1 Homo sapiens 82-85 33431858-6 2021 We further demonstrated that ABCA8 mediates the efflux of TCA out of PC cells, and that extracellular TCA activates extracellular signal-regulated kinase (ERK) signaling via the sphingosine 1-phosphate receptor 2 (S1PR2), which is responsible for ABCA8-induced GEM ineffectiveness. gemcitabine 261-264 mitogen-activated protein kinase 1 Homo sapiens 155-158 34490236-7 2021 Indeed, knockdown of CIRBP sensitized pancreatic tumors to gemcitabine treatment by diminishing DYRK1B expression and increasing the ratio of ERK/p38 activity. gemcitabine 59-70 mitogen-activated protein kinase 1 Homo sapiens 142-145 35165514-7 2022 Mechanistically, gemcitabine and XCT790 suppressed PC by inhibiting ERRalpha and MEK/ERK signaling pathway. gemcitabine 17-28 mitogen-activated protein kinase 1 Homo sapiens 85-88 33744388-5 2021 Additionally, co-treatment with RT22-ep59 and gemcitabine synergistically inhibited cell viability, migration, and invasion in 3D-cultures and exhibited synergistic anticancer activity by inhibiting the RAF/ERK or PI3K/AKT pathways in cells with high-EpCAM expression. gemcitabine 46-57 mitogen-activated protein kinase 1 Homo sapiens 207-210 33184874-0 2021 ERK-mediated transcriptional activation of Dicer is involved in gemcitabine resistance of pancreatic cancer. gemcitabine 64-75 mitogen-activated protein kinase 1 Homo sapiens 0-3 33184874-6 2021 Moreover, we identified that transcriptional factor Sp1 targeted the promoter region of Dicer and found ERK/Sp1 signaling regulated Dicer expression in PANC-1/GEM cells, as well as positively correlated with pancreatic cancer progression and suggest that targeting the ERK/Sp1/Dicer pathway has potential therapeutic value for pancreatic cancer with acquired resistance to gemcitabine. gemcitabine 373-384 mitogen-activated protein kinase 1 Homo sapiens 104-107 33184874-6 2021 Moreover, we identified that transcriptional factor Sp1 targeted the promoter region of Dicer and found ERK/Sp1 signaling regulated Dicer expression in PANC-1/GEM cells, as well as positively correlated with pancreatic cancer progression and suggest that targeting the ERK/Sp1/Dicer pathway has potential therapeutic value for pancreatic cancer with acquired resistance to gemcitabine. gemcitabine 373-384 mitogen-activated protein kinase 1 Homo sapiens 269-272 33662667-0 2021 Suppression of Wnt/beta-catenin and RAS/ERK pathways provides a therapeutic strategy for gemcitabine-resistant pancreatic cancer. gemcitabine 89-100 mitogen-activated protein kinase 1 Homo sapiens 40-43 33662667-5 2021 Gemcitabine treatment activates both the Wnt/beta-catenin and RAS/ERK pathways. gemcitabine 0-11 mitogen-activated protein kinase 1 Homo sapiens 66-69 33662667-11 2021 Overall, we demonstrated that inhibiting the Wnt/beta-catenin and RAS/ERK pathways by destabilizing beta-catenin and RAS could be a therapeutic approach to overcome gemcitabine resistance in pancreatic cancer. gemcitabine 165-176 mitogen-activated protein kinase 1 Homo sapiens 70-73 33878513-5 2021 RESULTS: We found that CUDC-101 and gemcitabine interacted synergistically to reduce NHL cell viability and to induce the apoptotic death of these cells via the EGFR/ PI3K/Akt and Erk pathways, which were regulated by HDAC signaling pathways. gemcitabine 36-47 mitogen-activated protein kinase 1 Homo sapiens 180-183 31602254-7 2019 Furthermore, FOXD1 is a direct target of miR-30a-5p and the miR-30a-5p/FOXD1/ERK axis may play an important role in the development of gemcitabine resistance in pancreatic cancer. gemcitabine 135-146 mitogen-activated protein kinase 1 Homo sapiens 77-80 32924987-8 2021 Gene set variation analysis (GSVA) showed that activity in the cell cycle/mitotic, ERBB, and ERK/MAPK pathways was higher in the high-risk compared with the low-risk group, which may lead to differences in OS.Interestingly, we observed that patients in the high-risk group were more sensitive to gemcitabine and docetaxel than the low-risk group, which is consistent with results of the GSVA. gemcitabine 296-307 mitogen-activated protein kinase 1 Homo sapiens 93-96 33288882-9 2021 Moreover, afatinib alone or in combination with gemcitabine decreased stemness and tumorspheres by reducing phosphorylation of EGFR family proteins, ERK, FAK, and CSC markers. gemcitabine 48-59 mitogen-activated protein kinase 1 Homo sapiens 149-152 32615164-0 2020 LLGL1 regulates gemcitabine resistance by modulating ERK-SP1-OSMR pathway in pancreatic ductal adenocarcinoma. gemcitabine 16-27 mitogen-activated protein kinase 1 Homo sapiens 53-56 31373074-4 2019 We show that gemcitabine-resistant Panc-1 and MiaPaca-2 cells of mesenchymal-like phenotype undergo further EMT-like molecular changes mediated by ERK-ZEB-1 pathway, and that inhibition of ERK1/2 phosphorylation or ZEB-1 expression resulted in a decrease in chemoresistance. gemcitabine 13-24 mitogen-activated protein kinase 1 Homo sapiens 147-150