PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27692847-6 2017 However, we found a striking down-regulation of activated ERK1/2 together with enhanced cytotoxicity in both docetaxel or cabazitaxel-treated cells that was comparable to direct MEK kinase inhibition. Docetaxel 109-118 mitogen-activated protein kinase 3 Homo sapiens 58-64 32179814-7 2020 Besides, melatonin prevented the positive actions that docetaxel exerts on the expression of other factors related to angiogenesis like JAG1, ANPEP, IGF-1, CXCL6, AKT1, ERK1, ERK2, MMP14 and NOS3 and neutralized the stimulating actions of vinorelbine on the expression of FIGF, FGFR3, CXCL6, CCL2, ERK1, ERK2, AKT1, NOS3 and MMP14. Docetaxel 55-64 mitogen-activated protein kinase 3 Homo sapiens 169-173 32179814-7 2020 Besides, melatonin prevented the positive actions that docetaxel exerts on the expression of other factors related to angiogenesis like JAG1, ANPEP, IGF-1, CXCL6, AKT1, ERK1, ERK2, MMP14 and NOS3 and neutralized the stimulating actions of vinorelbine on the expression of FIGF, FGFR3, CXCL6, CCL2, ERK1, ERK2, AKT1, NOS3 and MMP14. Docetaxel 55-64 mitogen-activated protein kinase 3 Homo sapiens 298-302 26821209-4 2016 In docetaxel-treated MDA-MB-231 cells, phosphorylated-ERK1/2 levels were increased by 60% in membrane and nuclear compartments, compared to untreated cells. Docetaxel 3-12 mitogen-activated protein kinase 3 Homo sapiens 54-60 26821209-5 2016 Our data showed that ERK1/2 activation depended on PKC activation since: i) enzastaurin (a pan-PKC inhibitor) blocked docetaxel-induced ERK1/2 phosphorylation ii) docetaxel increased PKC activity by 30% and phosphatidic acid level by 1.6-fold iii) inhibition of PKCepsilon and PKCdelta by siRNA resulted in reduced phosphorylated ERK1/2 levels. Docetaxel 118-127 mitogen-activated protein kinase 3 Homo sapiens 21-27 26821209-5 2016 Our data showed that ERK1/2 activation depended on PKC activation since: i) enzastaurin (a pan-PKC inhibitor) blocked docetaxel-induced ERK1/2 phosphorylation ii) docetaxel increased PKC activity by 30% and phosphatidic acid level by 1.6-fold iii) inhibition of PKCepsilon and PKCdelta by siRNA resulted in reduced phosphorylated ERK1/2 levels. Docetaxel 118-127 mitogen-activated protein kinase 3 Homo sapiens 136-142 26821209-5 2016 Our data showed that ERK1/2 activation depended on PKC activation since: i) enzastaurin (a pan-PKC inhibitor) blocked docetaxel-induced ERK1/2 phosphorylation ii) docetaxel increased PKC activity by 30% and phosphatidic acid level by 1.6-fold iii) inhibition of PKCepsilon and PKCdelta by siRNA resulted in reduced phosphorylated ERK1/2 levels. Docetaxel 118-127 mitogen-activated protein kinase 3 Homo sapiens 136-142 26821209-5 2016 Our data showed that ERK1/2 activation depended on PKC activation since: i) enzastaurin (a pan-PKC inhibitor) blocked docetaxel-induced ERK1/2 phosphorylation ii) docetaxel increased PKC activity by 30% and phosphatidic acid level by 1.6-fold iii) inhibition of PKCepsilon and PKCdelta by siRNA resulted in reduced phosphorylated ERK1/2 levels. Docetaxel 163-172 mitogen-activated protein kinase 3 Homo sapiens 21-27 26821209-6 2016 In DHA-supplemented cells, docetaxel was unable to increase PKCepsilon and delta levels in membrane and nuclear fractions, resulting in diminished ERK1/2 phosphorylation and increased docetaxel efficacy. Docetaxel 27-36 mitogen-activated protein kinase 3 Homo sapiens 147-153 24316750-7 2013 We further established that recombinant IL-17A recruits the MAPK pathway by upregulating phosphorylated ERK1/2 in human breast cancer cell lines thereby promoting proliferation and resistance to conventional chemotherapeutic agents such as docetaxel. Docetaxel 240-249 mitogen-activated protein kinase 3 Homo sapiens 60-64 26909952-7 2016 In addition, based on network analysis using the ingenuity pathway analysis software, DOX was found to suppress phosphorylation of extracellular signal-regulated kinase 1/2 and p38, suggesting that the mitogen-activated protein kinase signaling pathway plays a vital role in the anti-proliferative effect of DOX against RCC. Docetaxel 86-89 mitogen-activated protein kinase 3 Homo sapiens 131-172 26909952-7 2016 In addition, based on network analysis using the ingenuity pathway analysis software, DOX was found to suppress phosphorylation of extracellular signal-regulated kinase 1/2 and p38, suggesting that the mitogen-activated protein kinase signaling pathway plays a vital role in the anti-proliferative effect of DOX against RCC. Docetaxel 308-311 mitogen-activated protein kinase 3 Homo sapiens 131-172 24316750-7 2013 We further established that recombinant IL-17A recruits the MAPK pathway by upregulating phosphorylated ERK1/2 in human breast cancer cell lines thereby promoting proliferation and resistance to conventional chemotherapeutic agents such as docetaxel. Docetaxel 240-249 mitogen-activated protein kinase 3 Homo sapiens 104-110 23788635-8 2013 Thus, docetaxel treatment constitutively activated the CXCR4, ERK1/2, and c-Myc signaling loop in docetaxel-resistant residual prostate cancer cells. Docetaxel 98-107 mitogen-activated protein kinase 3 Homo sapiens 62-68 23788635-0 2013 Residual prostate cancer cells after docetaxel therapy increase the tumorigenic potential via constitutive signaling of CXCR4, ERK1/2 and c-Myc. Docetaxel 37-46 mitogen-activated protein kinase 3 Homo sapiens 127-133 23788635-5 2013 In docetaxel-treated DU145 cells, transiently activated ERK1/2 induced CXCR4 expression by stabilizing c-Myc. Docetaxel 3-12 mitogen-activated protein kinase 3 Homo sapiens 56-62 23788635-6 2013 Furthermore, constitutive activation of CXCR4, ERK1/2, and c-Myc signaling was evident in clinical tissue samples from human patients with docetaxel-resistant prostate cancer. Docetaxel 139-148 mitogen-activated protein kinase 3 Homo sapiens 47-53 23788635-8 2013 Thus, docetaxel treatment constitutively activated the CXCR4, ERK1/2, and c-Myc signaling loop in docetaxel-resistant residual prostate cancer cells. Docetaxel 6-15 mitogen-activated protein kinase 3 Homo sapiens 62-68 21798065-4 2011 RESULTS: 1) Treatment with ulinastatin, docetaxel, and ulinastatin plus docetaxel, respectively, significantly inhibited MDA-MB-231 and MCF-7 cell invasion; 2) mRNA and protein levels of uPA, uPAR and ERK1/2 were inhibited by ulinastatin, but enhanced by docetaxel. Docetaxel 40-49 mitogen-activated protein kinase 3 Homo sapiens 201-207 21455800-9 2012 Both docetaxel and sunitinib malate had no effect on each other in inhibiting ERK1/2 phosphorylation in sequential treatments, while docetaxel eliminated inhibitory activity of sunitinib malate on ERK1/2 phosphorylation in concurrent treatment. Docetaxel 133-142 mitogen-activated protein kinase 3 Homo sapiens 197-203 21798065-4 2011 RESULTS: 1) Treatment with ulinastatin, docetaxel, and ulinastatin plus docetaxel, respectively, significantly inhibited MDA-MB-231 and MCF-7 cell invasion; 2) mRNA and protein levels of uPA, uPAR and ERK1/2 were inhibited by ulinastatin, but enhanced by docetaxel. Docetaxel 72-81 mitogen-activated protein kinase 3 Homo sapiens 201-207 21798065-4 2011 RESULTS: 1) Treatment with ulinastatin, docetaxel, and ulinastatin plus docetaxel, respectively, significantly inhibited MDA-MB-231 and MCF-7 cell invasion; 2) mRNA and protein levels of uPA, uPAR and ERK1/2 were inhibited by ulinastatin, but enhanced by docetaxel. Docetaxel 72-81 mitogen-activated protein kinase 3 Homo sapiens 201-207 17317842-5 2007 RESULTS: Docetaxel induced activation of both JNK and ERK1/2 but not p38 mitogen-activated protein kinase or Akt kinases. Docetaxel 9-18 mitogen-activated protein kinase 3 Homo sapiens 54-60 21685708-6 2011 Docetaxel significantly inhibited the phosphorylation of extracellular signal-regulated kinase 1/2, Akt, and phospholipase C-gamma1, downstream molecule in the PDGF-BB signaling pathway. Docetaxel 0-9 mitogen-activated protein kinase 3 Homo sapiens 57-98 20664934-8 2010 DOC resistance in spheroids was reversed by inhibition of ERK1/2, but not of Akt, suggesting an important role for ERK1/2 in the DOC resistance in MCF-7 spheroids. Docetaxel 0-3 mitogen-activated protein kinase 3 Homo sapiens 58-64 20664934-8 2010 DOC resistance in spheroids was reversed by inhibition of ERK1/2, but not of Akt, suggesting an important role for ERK1/2 in the DOC resistance in MCF-7 spheroids. Docetaxel 0-3 mitogen-activated protein kinase 3 Homo sapiens 115-121 20664934-8 2010 DOC resistance in spheroids was reversed by inhibition of ERK1/2, but not of Akt, suggesting an important role for ERK1/2 in the DOC resistance in MCF-7 spheroids. Docetaxel 129-132 mitogen-activated protein kinase 3 Homo sapiens 58-64 20664934-8 2010 DOC resistance in spheroids was reversed by inhibition of ERK1/2, but not of Akt, suggesting an important role for ERK1/2 in the DOC resistance in MCF-7 spheroids. Docetaxel 129-132 mitogen-activated protein kinase 3 Homo sapiens 115-121 17317842-8 2007 In contrast, activation of ERK1/2 by docetaxel inhibited apoptosis and the levels of activation in individual lines were inversely correlated to the degree of apoptosis. Docetaxel 37-46 mitogen-activated protein kinase 3 Homo sapiens 27-33