PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23028726-5 2012 Doxorubicin treatment showed the following dose-dependent effects: increase in the secretion of tumor necrosis factor alpha; decrease in the expression of phosphorylated protein kinase A and Bcl-2; and increase in the expression of phosphorylated signal transducer and activator of transcription 3, phosphorylated extracellular signal-regulated kinase (ERK), and ATF3. Doxorubicin 0-11 mitogen-activated protein kinase 1 Homo sapiens 314-351 23028726-5 2012 Doxorubicin treatment showed the following dose-dependent effects: increase in the secretion of tumor necrosis factor alpha; decrease in the expression of phosphorylated protein kinase A and Bcl-2; and increase in the expression of phosphorylated signal transducer and activator of transcription 3, phosphorylated extracellular signal-regulated kinase (ERK), and ATF3. Doxorubicin 0-11 mitogen-activated protein kinase 1 Homo sapiens 353-356 23028726-6 2012 Based on these results, we suggest that doxorubicin induces cytotoxicity through an ERK-dependent pathway, and ATF3 plays a pivotal role as a transcriptional regulator in this process. Doxorubicin 40-51 mitogen-activated protein kinase 1 Homo sapiens 84-87 21854868-3 2011 Doxorubicin-induced caspase-8 activation was found to be mediated through Akt/ERK inactivation and FasL-independent Fas pathway in MCF-7 cells, while caspase-8 activation in MCF-7/Dox cells depended exclusively on FasL-stimulated Fas pathway. Doxorubicin 0-11 mitogen-activated protein kinase 1 Homo sapiens 78-81 21854868-3 2011 Doxorubicin-induced caspase-8 activation was found to be mediated through Akt/ERK inactivation and FasL-independent Fas pathway in MCF-7 cells, while caspase-8 activation in MCF-7/Dox cells depended exclusively on FasL-stimulated Fas pathway. Doxorubicin 0-3 mitogen-activated protein kinase 1 Homo sapiens 78-81 21854868-10 2011 Taken together, our data indicate that Akt/ERK-mediated caspase-8 activation and Fas/FasL-mediated caspase-8 activation mostly elucidate doxorubicin-induced death in MCF-7 cells and MCF-7/Dox cells, respectively. Doxorubicin 137-148 mitogen-activated protein kinase 1 Homo sapiens 43-46 21869603-5 2011 We have determined that chemotherapeutic drugs such as doxorubicin or the hormone based drug tamoxifen, both used to treat breast cancer, resulted in the activation of the Raf/MEK/ERK pathway which is often associated with a pro-proliferative, anti-apoptotic response. Doxorubicin 55-66 mitogen-activated protein kinase 1 Homo sapiens 180-183 21869603-6 2011 In drug sensitive MCF-7 cells which have wild-type p53; ERK, p53 and downstream p21 (Cip-1 ) were induced upon exposure to doxorubicin. Doxorubicin 123-134 mitogen-activated protein kinase 1 Homo sapiens 56-59 21300134-14 2011 CONCLUSION: Doxorubicin can increase expression of mdr1/P-glycoprotein through activating MAPK/ERK transduction pathway, then increasing expression of YB-1, inducing YB-1 nuclear translocation, and enhancing DNA-binding activity of YB-1. Doxorubicin 12-23 mitogen-activated protein kinase 1 Homo sapiens 95-98 21790999-3 2011 Because DOX causes cell death through upregulation of the MEK/ERK pathway, and sorafenib has an opposite influence on the same cascade, we hypothesized that co-treatment with these drugs may lead to an antagonistic effect. Doxorubicin 8-11 mitogen-activated protein kinase 1 Homo sapiens 62-65 21790999-9 2011 Similarly, ERK targeting with the selective inhibitor U0126 impaired DOX-induced toxicity. Doxorubicin 69-72 mitogen-activated protein kinase 1 Homo sapiens 11-14 21790999-12 2011 In conclusion, MEK/ERK counteraction, stimulation of survival via Akt and dysregulation of cyclin D1 could contribute to the escape from DOX-induced autophagy and thus promote cancer cell survival. Doxorubicin 137-140 mitogen-activated protein kinase 1 Homo sapiens 19-22 21881167-8 2011 However, constitutive Akt-1 activation in drug-resistant cells containing high levels of active ERK completely escaped cellular senescence induced by doxorubicin and tamoxifen. Doxorubicin 150-161 mitogen-activated protein kinase 1 Homo sapiens 96-99 21472291-6 2010 Akt and ERK activation was also detected, and the inhibition of these two pathways resulted in the enhancement of ADM-induced apoptosis. Doxorubicin 114-117 mitogen-activated protein kinase 1 Homo sapiens 8-11 21159167-0 2010 Blocking of ERK1 and ERK2 sensitizes human mesothelioma cells to doxorubicin. Doxorubicin 65-76 mitogen-activated protein kinase 1 Homo sapiens 21-25 18974122-8 2008 The phosphorylation of Akt and extracellular signal-regulated kinase 1/2 (ERK1/2) is elevated in Cas-overexpressing cells treated with Adriamycin, whereas expression of the proapoptotic protein Bak is decreased. Doxorubicin 135-145 mitogen-activated protein kinase 1 Homo sapiens 31-72 18468633-0 2008 The effect of doxorubicin on MEK-ERK signaling predicts its efficacy in HCC. Doxorubicin 14-25 mitogen-activated protein kinase 1 Homo sapiens 33-36 18468633-7 2008 At early time points (30 min) after DOX treatment of Hep3B cells, MEK activity was unchanged at low doses and decreased at higher doses; after 24 h, phospho-ERK levels increased at higher doses. Doxorubicin 36-39 mitogen-activated protein kinase 1 Homo sapiens 157-160 18468633-8 2008 Contrarily, in HepG2 cells, DOX caused a sustained, dose-dependent increase in phospho-ERK levels at early and late time points. Doxorubicin 28-31 mitogen-activated protein kinase 1 Homo sapiens 87-90 20428768-0 2010 Low doses of ionizing radiation suppress doxorubicin-induced senescence-like phenotypes by activation of ERK1/2 and suppression of p38 kinase in MCF7 human breast cancer cells. Doxorubicin 41-52 mitogen-activated protein kinase 1 Homo sapiens 131-134 20428768-7 2010 The phosphorylations of both p38 MAP kinase and p53 induced by doxorubicin were suppressed by low doses of ionizing radiation. Doxorubicin 63-74 mitogen-activated protein kinase 1 Homo sapiens 29-32 20428768-10 2010 The results thus suggest that low doses of radiation suppress doxorubicin-induced replicative senescence through the inhibition of p38-dependent phosphorylation of p53 and by activation of ERK1/2, without genomic damage. Doxorubicin 62-73 mitogen-activated protein kinase 1 Homo sapiens 131-134 19417026-1 2009 PURPOSE: Mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) dephosphorylates mitogen-activated protein kinase [extracellular signal-regulated kinase (ERK), c-Jun NH(2)-terminal kinase (JNK), and p38], mediates breast cancer chemoresistance, and is repressible by doxorubicin in breast cancer cells. Doxorubicin 274-285 mitogen-activated protein kinase 1 Homo sapiens 122-159 19417026-3 2009 EXPERIMENTAL DESIGN: Doxorubicin effects on MKP-1, phospho-ERK1/2 (p-ERK1/2), phospho-JNK (p-JNK), and phospho-p38 were assayed in a panel of human breast cancer cells by Western blot and in human breast cancer were assayed ex vivo by immunohistochemistry (n = 50). Doxorubicin 21-32 mitogen-activated protein kinase 1 Homo sapiens 111-114 19223549-7 2009 This XIAP-dependent event occurs in response to camptotechin or etoposide/VP16; however, XIAP is dispensable for activation of NF-kappaB by doxorubicin, which engages a MEK-ERK pathway to activate IKK. Doxorubicin 140-151 mitogen-activated protein kinase 1 Homo sapiens 173-176 18256541-7 2008 Prolonged treatment with two commonly-used chemotoxic compounds, doxorubicin and paclitaxel, caused increased activation of ERK in PTEN-positive DU145 cells, but not PTEN-negative PC3 cells. Doxorubicin 65-76 mitogen-activated protein kinase 1 Homo sapiens 124-127 17658517-3 2007 Under senescence-inducing condition, decreased Erk phosphorylation was detected in caRhoA-transfected cells and inactivation of Erk, but not p38, prevented doxorubicin-induced cell senescence. Doxorubicin 156-167 mitogen-activated protein kinase 1 Homo sapiens 128-131 15870880-5 2005 To confirm these findings, the MAPK signal transduction cascade was activated with EGF and response to doxorubicin or paclitaxel was measured in the presence/absence of the MEK-specific inhibitor, U0126. Doxorubicin 103-114 mitogen-activated protein kinase 1 Homo sapiens 31-35 17384286-0 2006 Superoxide anions are involved in doxorubicin-induced ERK activation in hepatocyte cultures. Doxorubicin 34-45 mitogen-activated protein kinase 1 Homo sapiens 54-57 17384286-7 2006 In this work, we have determined the possible involvement of particular free radicals in DOX-induced ERK phosphorylation in hepatocyte cultures by using specific free radical scavengers. Doxorubicin 89-92 mitogen-activated protein kinase 1 Homo sapiens 101-104 16269455-8 2006 The results showed that OEA, through activation of Ras-Raf-1-Mek-Erk signaling, inhibited doxorubicin-induced apoptosis. Doxorubicin 90-101 mitogen-activated protein kinase 1 Homo sapiens 65-68 16428504-11 2006 Furthermore, 17-AAG depleted cellular contents of Akt, decreased extracellular signal-regulated kinase (ERK) phosphorylation, and reduced cellular FLICE-like inhibitory protein levels (FLIP), and thus enhanced the cytotoxic effect of doxorubicin and agonistic anti-tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptor antibodies. Doxorubicin 234-245 mitogen-activated protein kinase 1 Homo sapiens 65-102 15494689-6 2004 RESULTS: Our findings demonstrated that DOX treatment of the BL41 cells led to sustained activation of JNK1/2 and p38 MAPK. Doxorubicin 40-43 mitogen-activated protein kinase 1 Homo sapiens 114-117 15494689-1 2004 AIM: To understand the biochemical basis of cell sensitivity to cytotoxic effect of doxorubicine (DOX), we investigated signaling cascades mediated by c-Jun N-terminal protein kinases (JNK1/2), p38 mitogen-activated protein kinases (MAPK), extracellular signal-regulated protein kinase (ERK1/2) and protein kinase B/Akt in both DOX-sensitive BL41 and the DOX-resistant DG75 Burkitt"s lymphoma (BL) cell lines. Doxorubicin 84-96 mitogen-activated protein kinase 1 Homo sapiens 194-197 16059641-5 2005 Furthermore, treatments of both cell lines by QU and in its combined application with DOX increased phosphorylation of ERK, while Akt-1 and phosphorylated Akt-1 levels were not changed. Doxorubicin 86-89 mitogen-activated protein kinase 1 Homo sapiens 119-122 15494689-7 2004 This activation/phosphorylation did not result from increased expression of either JNK1/2 or p38 MAPK since protein levels of JNK1/2 and p38 MAPK in DOX-treated and untreated cells were unaltered. Doxorubicin 149-152 mitogen-activated protein kinase 1 Homo sapiens 137-140 15494689-9 2004 The effect of DOX in drug-resistant cell line DG75 convoyed by dephosphorylation of JNK1/2, p38 MAPK and activation of Akt. Doxorubicin 14-17 mitogen-activated protein kinase 1 Homo sapiens 92-95 15494689-11 2004 CONCLUSION: The outcome of cellular response to DOX in BL cell lines is determined by interference of at least three signaling pathways: JNK1/2, p38 MAPK and PKB/Akt. Doxorubicin 48-51 mitogen-activated protein kinase 1 Homo sapiens 145-148 15116093-0 2004 Phosphorylation of p53 on Thr55 by ERK2 is necessary for doxorubicin-induced p53 activation and cell death. Doxorubicin 57-68 mitogen-activated protein kinase 1 Homo sapiens 35-39 15116093-1 2004 We recently reported that exposure of human cervical carcinoma cells to doxorubicin results in extracellular signal-regulated kinase (ERK)2 activation, which in turn phosphorylates p53 on a previously uncharacterized site, Thr55. Doxorubicin 72-83 mitogen-activated protein kinase 1 Homo sapiens 95-139 14755690-7 2004 Inhibition of PI 3K/Akt and p38 accelerated and enhanced doxorubicin-induced cell death. Doxorubicin 57-68 mitogen-activated protein kinase 1 Homo sapiens 28-31 14755690-10 2004 Activation of PI 3K/Akt and p38 modulates apoptotic signal pathways and inhibits doxorubicin-induced cell death. Doxorubicin 81-92 mitogen-activated protein kinase 1 Homo sapiens 28-31 12907245-0 2003 The JNK, ERK and p53 pathways play distinct roles in apoptosis mediated by the antitumor agents vinblastine, doxorubicin, and etoposide. Doxorubicin 109-120 mitogen-activated protein kinase 1 Homo sapiens 9-12 15116093-3 2004 In breast carcinoma MCF7 cells, doxorubicin (300 nM) activated ERK2 and induced phosphorylation of p53 on Thr55 residues. Doxorubicin 32-43 mitogen-activated protein kinase 1 Homo sapiens 63-67 15116093-4 2004 Pretreatment of MCF7 cells with an ERK2 chemical inhibitor, PD98059 or U0126, blocked doxorubicin-induced p53 activation and suppressed phosphorylation of p53Thr55. Doxorubicin 86-97 mitogen-activated protein kinase 1 Homo sapiens 35-39 15116093-9 2004 In summary, our results suggest that phosphorylation of p53Thr55 by ERK2 is important for doxorubicin-induced p53 activation and cell death. Doxorubicin 90-101 mitogen-activated protein kinase 1 Homo sapiens 68-72 12907245-8 2003 Inhibition of ERK signaling by the MEK inhibitor, U0126, potentiated the cytotoxic effects of vinblastine and doxorubicin, but not that of VP-16. Doxorubicin 110-121 mitogen-activated protein kinase 1 Homo sapiens 14-17 11996883-1 2002 In this study, we showed that suppression of the MEK-ERK transduction pathway by a selective inhibitor, 2"-amino-3"-methoxyflavone (PD98059), increased drug resistance of SiHa cells to cisplatin, but not to another common anticancer drug, doxorubicin. Doxorubicin 239-250 mitogen-activated protein kinase 1 Homo sapiens 53-56 12394272-7 2002 Interestingly, treatment with EBPC in combination with the chemotherapeutic drugs increased ERK activity as compared to treatment with the chemotherapeutic drugs, suggesting a possible role for the ERK pathway in mediating doxorubicin- or cisplatin-induced cell death. Doxorubicin 223-234 mitogen-activated protein kinase 1 Homo sapiens 92-95 12394272-7 2002 Interestingly, treatment with EBPC in combination with the chemotherapeutic drugs increased ERK activity as compared to treatment with the chemotherapeutic drugs, suggesting a possible role for the ERK pathway in mediating doxorubicin- or cisplatin-induced cell death. Doxorubicin 223-234 mitogen-activated protein kinase 1 Homo sapiens 198-201 12883037-5 2003 We identified that serum starvation and Dox reduced phosphorylation of mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase (MEK), protein kinase C (PKC) alpha/beta and c-Jun NH(2)-terminal kinase. Doxorubicin 40-43 mitogen-activated protein kinase 1 Homo sapiens 143-146 12883037-7 2003 Thus, our data suggest that apoptosis and down-regulation of XIAP induced by Dox exposure or serum starvation may be mediated through inactivation of the MEK/ERK and PKCalpha/beta pathways. Doxorubicin 77-80 mitogen-activated protein kinase 1 Homo sapiens 158-161 11996883-3 2002 Both cisplatin and doxorubicin activated nuclear ERK2 and nuclear transcription factor kappa B (NF kappa B) of SiHa cells. Doxorubicin 19-30 mitogen-activated protein kinase 1 Homo sapiens 49-53 33771646-5 2021 While doxorubicin was identified to activate the pathways TGF-beta and ERK/MAPK, lercanidipinewas found to inhibit these pathways. Doxorubicin 6-17 mitogen-activated protein kinase 1 Homo sapiens 71-74 11409876-0 2001 Nuclear extracellular signal-regulated kinase 2 phosphorylates p53 at Thr55 in response to doxorubicin. Doxorubicin 91-102 mitogen-activated protein kinase 1 Homo sapiens 8-47 11409876-1 2001 In this study, we showed that nuclear ERK2 phosphorylates p53 at Thr55 in response to doxorubicin. Doxorubicin 86-97 mitogen-activated protein kinase 1 Homo sapiens 38-42 11170175-7 2001 Doxorubicin (0.2 microM), an anticancer drug whose mechanism of action is independent of microtubules, also induced ERK activation, tau phosphorylation and apoptosis. Doxorubicin 0-11 mitogen-activated protein kinase 1 Homo sapiens 116-119 8913269-1 1996 We studied the activation of c-jun N-terminal kinase 1 (JNK 1) and extracellular signal-regulated kinases 1 and 2 (ERK 1/2) of mitogen-activated protein kinase (MAPK) family by adriamycin (ADR) in the human T cell leukemia line, H9. Doxorubicin 177-187 mitogen-activated protein kinase 1 Homo sapiens 67-113 33771646-7 2021 In multiple cellular models from different lineages, the cells with less sensitivity to doxorubicin were found to have the inherent activation of ERK/MAPK and TGF-beta pathways. Doxorubicin 88-99 mitogen-activated protein kinase 1 Homo sapiens 146-149 34232382-11 2021 479 differentially expressed genes were identified between HL60-EIF2S3 DOX (-) and HL60-EIF2S3 DOX ( +) cells via NGS and several of them involved in MAPK/ERK signaling pathway. Doxorubicin 71-74 mitogen-activated protein kinase 1 Homo sapiens 155-158 34783124-7 2022 Furthermore, the polymerase chain reaction array results illustrate activation of mitogen-activated protein kinase (MAPK) gene expression (AKT, ERK, and MAPK) during doxorubicin alone treatment and it has been attenuated by ginsenoside Rg1 pretreatment. Doxorubicin 166-177 mitogen-activated protein kinase 1 Homo sapiens 144-147 34232382-11 2021 479 differentially expressed genes were identified between HL60-EIF2S3 DOX (-) and HL60-EIF2S3 DOX ( +) cells via NGS and several of them involved in MAPK/ERK signaling pathway. Doxorubicin 95-98 mitogen-activated protein kinase 1 Homo sapiens 155-158 34520240-0 2021 Retraction of: miR-132 Regulates Adriamycin Resistance in Colorectal Cancer Cells Through Targeting Extracellular Signal-Regulated Kinase 1 (doi: 10.1089/cbr.2018.2749). Doxorubicin 33-43 mitogen-activated protein kinase 1 Homo sapiens 100-139 35395977-9 2022 CONCLUSION: DOX can induce apoptosis of H929 via intrinsic apoptosis pathway, and MEK/ERK pathway and c-Jun possibly play a role in this process. Doxorubicin 12-15 mitogen-activated protein kinase 1 Homo sapiens 86-89 34119884-3 2021 Herein, we developed a nanovector Exo-PMA/Fe-HSA@DOX through cloaked by urinary exosome membrane as a chemo/chemodynamic theranostic nano-platform for targeted homologous prostate cancer therapy which pertain to the abrogation of Epidermal Growth Factor Receptor (EGFR) and its downstream AKT/NF-kB/IkB signaling instead of ERK signaling cascades. Doxorubicin 49-52 mitogen-activated protein kinase 1 Homo sapiens 324-327 34589399-0 2021 Combination therapy with miR34a and doxorubicin synergistically inhibits Dox-resistant breast cancer progression via down-regulation of Snail through suppressing Notch/NF-kappaB and RAS/RAF/MEK/ERK signaling pathway. Doxorubicin 36-47 mitogen-activated protein kinase 1 Homo sapiens 194-197 34589399-0 2021 Combination therapy with miR34a and doxorubicin synergistically inhibits Dox-resistant breast cancer progression via down-regulation of Snail through suppressing Notch/NF-kappaB and RAS/RAF/MEK/ERK signaling pathway. Doxorubicin 73-76 mitogen-activated protein kinase 1 Homo sapiens 194-197 34589399-14 2021 What" more, for the first time, we also found miR34a combined with Dox could obviously inhibit the expression of Snail through suppressing Notch/NF-kappaB and RAS/RAF/MEK/ERK pathway in MCF-7/A cells. Doxorubicin 67-70 mitogen-activated protein kinase 1 Homo sapiens 171-174 34238921-13 2021 Syncytin-1 suppressed doxorubicin-induced apoptosis via MEK/ERK cascade. Doxorubicin 22-33 mitogen-activated protein kinase 1 Homo sapiens 60-63 35209071-5 2022 Therefore, we investigated the effects of UA on invasion and metastasis, ODC-related polyamine metabolism, and MAPK-Erk-VEGF/MMP-9 signaling pathways in a doxorubicin-resistant breast cancer cell (MCF-7/ADR) model. Doxorubicin 155-166 mitogen-activated protein kinase 1 Homo sapiens 116-119 31377057-2 2019 Here, we identified the regulation of mammalian target of rapamycin complex1 (mTORC1) by TGF-beta via extracellular signal-regulated kinase-1/2 (ERK1/2) in the Adriamycin (ADR)-induced murine model of focal segmental glomerulosclerosis. Doxorubicin 160-170 mitogen-activated protein kinase 1 Homo sapiens 102-143 35039569-10 2022 In cell lines, mutant RASGRP4 increased basal p-ERK expression and lead to a growth advantage in colony forming assays when challenged with doxorubicin. Doxorubicin 140-151 mitogen-activated protein kinase 1 Homo sapiens 48-51 33115283-4 2021 In vitro assay, ROSI significantly enhanced the inhibitory effects of adriamycin (ADR) on the proliferation, autophagy and migration of insulin-resistant hepatoma HepG2/IR cells via downregulation of EGFR/ERK and AKT/mTOR signaling pathway. Doxorubicin 70-80 mitogen-activated protein kinase 1 Homo sapiens 205-208 32818507-8 2020 Mechanistically, EGCG reduced ERK phosphorylation concentration-dependently, and sensitized gemcitabine, 5-FU, and doxorubicin to further suppress ERK phosphorylation in multiple cancer cell lines. Doxorubicin 115-126 mitogen-activated protein kinase 1 Homo sapiens 147-150 32722178-4 2020 In doxorubicin-treated H9c2 cardiomyoblasts, the long-lasting cardioprotection is mediated by activation of the Ras/Raf/Mek/Erk (extracellular signal-regulated kinase 1,2) signaling pathway and requires Stat3 (signal transducer and activator of transcription 3) activation. Doxorubicin 3-14 mitogen-activated protein kinase 1 Homo sapiens 124-127 31843629-0 2020 Parameritannin A-2 from Urceola huaitingii enhances doxorubicin-induced mitochondria-dependent apoptosis by inhibiting the PI3K/Akt, ERK1/2 and p38 pathways in gastric cancer cells. Doxorubicin 52-63 mitogen-activated protein kinase 1 Homo sapiens 144-147 31843629-7 2020 Moreover, PA-2 attenuates the DOX-induced activation of Akt, ERK1/2 and p38 signaling pathways, providing a molecular mechanism for the synergistic effects of DOX and PA-2 in the induction of apoptosis. Doxorubicin 30-33 mitogen-activated protein kinase 1 Homo sapiens 72-75 31843629-7 2020 Moreover, PA-2 attenuates the DOX-induced activation of Akt, ERK1/2 and p38 signaling pathways, providing a molecular mechanism for the synergistic effects of DOX and PA-2 in the induction of apoptosis. Doxorubicin 159-162 mitogen-activated protein kinase 1 Homo sapiens 72-75 31843629-8 2020 In conclusion, our studies demonstrate that PA-2 and DOX synergistically induce mitochondria-dependent apoptosis as PA-2 inhibits the PI3K/Akt, ERK1/2 and p38 pathways in HGC27 cells. Doxorubicin 53-56 mitogen-activated protein kinase 1 Homo sapiens 155-158 32459053-11 2020 The activation of RasGRP1/Ras/ERK signaling might contribute to the Dox resistance effect of BRD2. Doxorubicin 68-71 mitogen-activated protein kinase 1 Homo sapiens 30-33 32354131-6 2020 The DOX-stimulated expression of IkappaBalpha, NF-kappaB, COX-2, and IL-8 were all downregulated by exercise as well as the fibrosis factors (TGF-beta1, phosphorylated ERK, Sp1, and CTGF). Doxorubicin 4-7 mitogen-activated protein kinase 1 Homo sapiens 168-171 31356549-9 2019 Further study indicated that curdione decreased DOX-induced phosphorylation of extracellular signal-regulated kinase1/2 (Erk1/2) and c-Jun-N-terminal kinase and activated nuclear factor-erythroid 2-related factor 2/heme oxygenase 1 (Nrf2/HO-1) signal pathway. Doxorubicin 48-51 mitogen-activated protein kinase 1 Homo sapiens 79-119 29574069-10 2018 It is important to note that the forskolin-induced potentiation of sensitivity to doxorubicin is accompanied by a strong inhibition of ERK1/2 phosphorylation, is mimicked by ERK inhibitor PD98059 and is prevented by pre-treatment with Protein Kinase A (PKA) and adenylate cyclase inhibitors. Doxorubicin 82-93 mitogen-activated protein kinase 1 Homo sapiens 135-138 30230033-13 2018 Whereas the inhibition of the MAPK pathway has the potential to inhibit chondrosarcoma cell migration, p38 inhibition, and ERK activation may render cells more sensitive to Dox. Doxorubicin 173-176 mitogen-activated protein kinase 1 Homo sapiens 123-126 29574069-11 2018 Altogether, our data indicate that forskolin sensitizes TNBC cells to doxorubicin via a mechanism depending on the cAMP/PKA-mediated ERK inhibition. Doxorubicin 70-81 mitogen-activated protein kinase 1 Homo sapiens 133-136 29108991-5 2018 In addition, MEK inhibitor (PD98059) blocked the SETDB1 regulation of the FosB promoter activity via ERK2 activation during doxorubicin treatment. Doxorubicin 124-135 mitogen-activated protein kinase 1 Homo sapiens 101-105 29307829-0 2018 Blockage of cytosolic phospholipase A2 alpha sensitizes aggressive breast cancer to doxorubicin through suppressing ERK and mTOR kinases. Doxorubicin 84-95 mitogen-activated protein kinase 1 Homo sapiens 116-119 28027688-8 2017 Treatment of DOX-resistant MDA-MB-435 cells with silibinin at 200 muM reduced DOX IC50 from 71 to 10 mug/mL and significantly suppressed the key oncogenic pathways including STAT3, AKT, and ERK in these cells. Doxorubicin 13-16 mitogen-activated protein kinase 1 Homo sapiens 190-193 28295305-10 2018 Taken together, we found that DOX induced mitochondrial ROS release to activate ERK-mediated HSF2 nuclear translocation and AT1 R upregulation causing DOX-damaged heart failure in vitro and in vivo. Doxorubicin 30-33 mitogen-activated protein kinase 1 Homo sapiens 80-83 28295305-10 2018 Taken together, we found that DOX induced mitochondrial ROS release to activate ERK-mediated HSF2 nuclear translocation and AT1 R upregulation causing DOX-damaged heart failure in vitro and in vivo. Doxorubicin 151-154 mitogen-activated protein kinase 1 Homo sapiens 80-83 29061787-0 2017 (-)-Epigallocatechin-3-gallate Down-regulates Doxorubicin-induced Overexpression of P-glycoprotein Through the Coordinate Inhibition of PI3K/Akt and MEK/ERK Signaling Pathways. Doxorubicin 46-57 mitogen-activated protein kinase 1 Homo sapiens 153-156 28923539-11 2017 In addition, we also demonstrated that angiogenesis inhibitory effect was mediated by DOX and VEGF triggered signal pathways, including PI3K/Akt, Raf/MEK/ERK, and adhesion related pathways. Doxorubicin 86-89 mitogen-activated protein kinase 1 Homo sapiens 154-157 29061787-7 2017 DOX induced the overexpression of MDR1 mRNA and increased the phosphorylation of Akt, ERK1/2, p38 MAPK and JNK. Doxorubicin 0-3 mitogen-activated protein kinase 1 Homo sapiens 94-97 29061787-11 2017 CONCLUSION: EGCG inhibited DOX-induced overexpression of P-gp through the coordinate inhibitory action on MEK/ERK and PI3K/Akt signaling pathways. Doxorubicin 27-30 mitogen-activated protein kinase 1 Homo sapiens 110-113 28988530-0 2017 Hyperexpression of Integrin alpha5beta1 Promotes Resistance of MCF-7 Human Breast Carcinoma Cells to Doxorubicin via ERK Protein Kinase Down-regulation. Doxorubicin 101-112 mitogen-activated protein kinase 1 Homo sapiens 117-120 28988530-4 2017 Diminished Erk activity accompanying the rise of drug resistance can be explained by an "atypical" function of this kinase, which, in the cells studied, promotes an enhanced rather than reduced sensitivity to doxorubicin. Doxorubicin 209-220 mitogen-activated protein kinase 1 Homo sapiens 11-14 28793338-8 2017 M-E5 enhanced the efficiency of Dox by down-regulating the phosphorylation level of Akt, Erk and p38/MAPK proteins. Doxorubicin 32-35 mitogen-activated protein kinase 1 Homo sapiens 89-92 27649518-6 2017 Dox and AD198 increased activation of AKT, ERK1/2, and p38 MAPK signaling pathways in tested OSCC cells by dose-dependent manner. Doxorubicin 0-3 mitogen-activated protein kinase 1 Homo sapiens 55-58 27649518-8 2017 Inhibition of PI3K/AKT reduced Dox- and AD198-induced activation of ERK1/2 and further increased Dox- and AD198-induced phosphorylation of p38 MAPK in OSCC. Doxorubicin 97-100 mitogen-activated protein kinase 1 Homo sapiens 139-142 28793338-8 2017 M-E5 enhanced the efficiency of Dox by down-regulating the phosphorylation level of Akt, Erk and p38/MAPK proteins. Doxorubicin 32-35 mitogen-activated protein kinase 1 Homo sapiens 101-105 28229963-0 2017 Constitutively activated ERK sensitizes cancer cells to doxorubicin: Involvement of p53-EGFR-ERK pathway. Doxorubicin 56-67 mitogen-activated protein kinase 1 Homo sapiens 25-28 28229963-4 2017 We investigated the involvement of activation of ERK signalling as a consequence of non-functional p53, in sensitivity of cells to doxorubicin. Doxorubicin 131-142 mitogen-activated protein kinase 1 Homo sapiens 49-52 28229963-0 2017 Constitutively activated ERK sensitizes cancer cells to doxorubicin: Involvement of p53-EGFR-ERK pathway. Doxorubicin 56-67 mitogen-activated protein kinase 1 Homo sapiens 93-96 26842910-18 2016 CONCLUSION: Our results indicate that miR-302 cooperatively sensitizes breast cancer cells to adriamycin via suppressing P-glycoprotein by targeting MEKK1 of ERK pathway. Doxorubicin 94-104 mitogen-activated protein kinase 1 Homo sapiens 158-161 28098907-0 2017 Synergistic combination of YS-1 and adriamycin inhibits human renal cancer through ERK1/2 signaling pathway in vitro and in vivo. Doxorubicin 36-46 mitogen-activated protein kinase 1 Homo sapiens 83-89 28098907-5 2017 We found that ADM monotherapy treatment notably upregulated the activity of extracellular signal-regulated kinase ERK1 and ERK2 (ERK1/2), but when combined with YS-1, the p-ERK1/2 level was reduced; then inhibited the Ras/Raf/MEK pathway. Doxorubicin 14-17 mitogen-activated protein kinase 1 Homo sapiens 123-127 28098907-5 2017 We found that ADM monotherapy treatment notably upregulated the activity of extracellular signal-regulated kinase ERK1 and ERK2 (ERK1/2), but when combined with YS-1, the p-ERK1/2 level was reduced; then inhibited the Ras/Raf/MEK pathway. Doxorubicin 14-17 mitogen-activated protein kinase 1 Homo sapiens 129-135 28098907-5 2017 We found that ADM monotherapy treatment notably upregulated the activity of extracellular signal-regulated kinase ERK1 and ERK2 (ERK1/2), but when combined with YS-1, the p-ERK1/2 level was reduced; then inhibited the Ras/Raf/MEK pathway. Doxorubicin 14-17 mitogen-activated protein kinase 1 Homo sapiens 173-179 25268131-0 2014 Urotensin II inhibits doxorubicin-induced human umbilical vein endothelial cell death by modulating ATF expression and via the ERK and Akt pathway. Doxorubicin 22-33 mitogen-activated protein kinase 1 Homo sapiens 127-130 25742496-0 2015 Correction: Urotensin II inhibits doxorubicin-induced human umbilical vein endothelial cell death by modulating ATF expression and via the ERK and Akt pathway. Doxorubicin 34-45 mitogen-activated protein kinase 1 Homo sapiens 139-142 25268131-12 2014 The inhibitory effect of U-II on DOX-increased apoptosis was attenuated by inhibitors of ERK (U0126) and PI3K/Akt (LY294002). Doxorubicin 33-36 mitogen-activated protein kinase 1 Homo sapiens 89-92 24797310-6 2014 Mechanistic studies indicated that this sensitization of SeC to DOX was achieved by triggering inactivation of ERK and AKT and DNA damage through reactive oxygen species (ROS) overproduction. Doxorubicin 64-67 mitogen-activated protein kinase 1 Homo sapiens 111-114 25043687-5 2014 In the sensitive K562 and HL60 cell lines, the changes of the p38 MAPK expression after the acidification are not as obvious as that of K562/DOX cells, but the activation of extracellular signal-regulated kinase (ERK) is also observed, which indicates that the down-regulation of p38 MAPK by the intracellular acidification might be the resistant cell line specific. Doxorubicin 141-144 mitogen-activated protein kinase 1 Homo sapiens 174-211 24830744-5 2014 Furthermore, our results indicated that EVO enhanced the apoptotic action of DOX by inhibiting the Ras/MEK/ERK cascade and the expression of IAPs without inhibiting the expression and activity of P-glycoprotein (P-gp). Doxorubicin 77-80 mitogen-activated protein kinase 1 Homo sapiens 107-110 24407515-8 2014 However, resistance to doxorubicin and tamoxifen were alleviated in MCF-7/GSK-3beta(KD) cells upon co-treatment with an MEK inhibitor, indicating regulation of this resistance by the Raf/MEK/ERK pathway. Doxorubicin 23-34 mitogen-activated protein kinase 1 Homo sapiens 191-194 24147064-9 2013 Finally, doxorubicin caused a significant elevation in the levels of signalling proteins p-Akt, p-Erk 1/2, p-Drp1 and p-p53. Doxorubicin 9-20 mitogen-activated protein kinase 1 Homo sapiens 98-105 23994249-0 2013 Chrysin enhances sensitivity of BEL-7402/ADM cells to doxorubicin by suppressing PI3K/Akt/Nrf2 and ERK/Nrf2 pathway. Doxorubicin 54-65 mitogen-activated protein kinase 1 Homo sapiens 99-102 23320839-11 2013 Treatment of gemcitabine or doxorubicin activated phosphorylated ERK and induced the upregulation of MRP1 and MRP3. Doxorubicin 28-39 mitogen-activated protein kinase 1 Homo sapiens 65-68 23320839-12 2013 MEK inhibitors U0126 and AZD6244 deactivated phosphorylated ERK, decreased endogenous MRP1 expression, reversed gemcitabine or doxorubicin induced MRP1 and MRP3 upregulation, and increased the intracellular doxorubicin accumulation. Doxorubicin 127-138 mitogen-activated protein kinase 1 Homo sapiens 60-63 22576950-9 2012 Western blot results showed the upregulation of phosphorylated protein kinase B (AKT) and phosphorylated extracellular signal-regulated protein kinase (ERK) in Adriamycin-sensitive SGC7901 cell by MDK transfection accompanied with drug resistance to ADR, although the level of AKT and ERK protein expression did not change, so our results suggested that MDK, which can activate AKT and ERK by phosphorylation, induced the Adriamycin resistance in gastric cancer cells. Doxorubicin 160-170 mitogen-activated protein kinase 1 Homo sapiens 105-150 24217648-7 2013 Moreover, doxorubicin markedly activated phosphorylated ERK, p38 and JNK proteins in BMSCs. Doxorubicin 10-21 mitogen-activated protein kinase 1 Homo sapiens 56-59 22576950-9 2012 Western blot results showed the upregulation of phosphorylated protein kinase B (AKT) and phosphorylated extracellular signal-regulated protein kinase (ERK) in Adriamycin-sensitive SGC7901 cell by MDK transfection accompanied with drug resistance to ADR, although the level of AKT and ERK protein expression did not change, so our results suggested that MDK, which can activate AKT and ERK by phosphorylation, induced the Adriamycin resistance in gastric cancer cells. Doxorubicin 160-170 mitogen-activated protein kinase 1 Homo sapiens 285-288 22576950-9 2012 Western blot results showed the upregulation of phosphorylated protein kinase B (AKT) and phosphorylated extracellular signal-regulated protein kinase (ERK) in Adriamycin-sensitive SGC7901 cell by MDK transfection accompanied with drug resistance to ADR, although the level of AKT and ERK protein expression did not change, so our results suggested that MDK, which can activate AKT and ERK by phosphorylation, induced the Adriamycin resistance in gastric cancer cells. Doxorubicin 422-432 mitogen-activated protein kinase 1 Homo sapiens 105-150 22576950-9 2012 Western blot results showed the upregulation of phosphorylated protein kinase B (AKT) and phosphorylated extracellular signal-regulated protein kinase (ERK) in Adriamycin-sensitive SGC7901 cell by MDK transfection accompanied with drug resistance to ADR, although the level of AKT and ERK protein expression did not change, so our results suggested that MDK, which can activate AKT and ERK by phosphorylation, induced the Adriamycin resistance in gastric cancer cells. Doxorubicin 160-170 mitogen-activated protein kinase 1 Homo sapiens 152-155 22576950-9 2012 Western blot results showed the upregulation of phosphorylated protein kinase B (AKT) and phosphorylated extracellular signal-regulated protein kinase (ERK) in Adriamycin-sensitive SGC7901 cell by MDK transfection accompanied with drug resistance to ADR, although the level of AKT and ERK protein expression did not change, so our results suggested that MDK, which can activate AKT and ERK by phosphorylation, induced the Adriamycin resistance in gastric cancer cells. Doxorubicin 422-432 mitogen-activated protein kinase 1 Homo sapiens 152-155 22576950-9 2012 Western blot results showed the upregulation of phosphorylated protein kinase B (AKT) and phosphorylated extracellular signal-regulated protein kinase (ERK) in Adriamycin-sensitive SGC7901 cell by MDK transfection accompanied with drug resistance to ADR, although the level of AKT and ERK protein expression did not change, so our results suggested that MDK, which can activate AKT and ERK by phosphorylation, induced the Adriamycin resistance in gastric cancer cells. Doxorubicin 160-170 mitogen-activated protein kinase 1 Homo sapiens 285-288 22429871-9 2012 In addition, Dox distinctly increased the phosphorylation of p38, JNK and ERK MAPKs. Doxorubicin 13-16 mitogen-activated protein kinase 1 Homo sapiens 74-77 22787275-5 2012 We also demonstrate that activation of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase signaling pathway is involved in collagen-induced reduction of intracellular doxorubicin accumulation, collagen-induced up-regulation of ABCC1 expression levels, and collagen-mediated cell survival. Doxorubicin 197-208 mitogen-activated protein kinase 1 Homo sapiens 43-80 22787275-5 2012 We also demonstrate that activation of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase signaling pathway is involved in collagen-induced reduction of intracellular doxorubicin accumulation, collagen-induced up-regulation of ABCC1 expression levels, and collagen-mediated cell survival. Doxorubicin 197-208 mitogen-activated protein kinase 1 Homo sapiens 82-85 22469513-0 2012 Mitochondrial superoxide mediates doxorubicin-induced keratinocyte apoptosis through oxidative modification of ERK and Bcl-2 ubiquitination. Doxorubicin 34-45 mitogen-activated protein kinase 1 Homo sapiens 111-114 22457358-0 2012 alpha2beta1 integrin promotes chemoresistance against doxorubicin in cancer cells through extracellular signal-regulated kinase (ERK). Doxorubicin 54-65 mitogen-activated protein kinase 1 Homo sapiens 90-127 22457358-7 2012 Furthermore, activation of MAPK/ERK, but not PI3K/AKT, is required for ColI-mediated inhibition of doxorubicin-induced JNK activation and apoptosis and for ColI-mediated maintenance of Mcl-1 levels. Doxorubicin 99-110 mitogen-activated protein kinase 1 Homo sapiens 32-35 22457358-0 2012 alpha2beta1 integrin promotes chemoresistance against doxorubicin in cancer cells through extracellular signal-regulated kinase (ERK). Doxorubicin 54-65 mitogen-activated protein kinase 1 Homo sapiens 129-132 22493363-9 2012 Doxorubicin caused up-regulation of phosphorylated ERK in T47D cells, which was not inhibited by NVP-AEW541. Doxorubicin 0-11 mitogen-activated protein kinase 1 Homo sapiens 51-54 23493035-0 2012 Different Expression of Extracellular Signal-Regulated Kinases (ERK) 1/2 and Phospho-Erk Proteins in MBA-MB-231 and MCF-7 Cells after Chemotherapy with Doxorubicin or Docetaxel. Doxorubicin 152-163 mitogen-activated protein kinase 1 Homo sapiens 24-72 23493035-0 2012 Different Expression of Extracellular Signal-Regulated Kinases (ERK) 1/2 and Phospho-Erk Proteins in MBA-MB-231 and MCF-7 Cells after Chemotherapy with Doxorubicin or Docetaxel. Doxorubicin 152-163 mitogen-activated protein kinase 1 Homo sapiens 85-88 23493035-9 2012 In MDA-MB-231 cells the expression of ERK1/2 and phospho-ERK was decreased after DOX treatment in a dose-dependent manner. Doxorubicin 81-84 mitogen-activated protein kinase 1 Homo sapiens 38-41 23493035-10 2012 In contrast in MCF-7 cells the expression of ERK1/2 and phospho-ERK was increased after DOX treatment. Doxorubicin 88-91 mitogen-activated protein kinase 1 Homo sapiens 45-48