PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24927258-0 2014 Increased growth-inhibitory and cytotoxic activity of arsenic trioxide in head and neck carcinoma cells with functional p53 deficiency and resistance to EGFR blockade. Arsenic Trioxide 54-70 epidermal growth factor receptor Homo sapiens 153-157 34189121-5 2021 Interaction of Arsenic trioxide (ATO) with EGFR signalling pathway factors has been elicited by systematic search in data bases, as ATO is one of the mysterious chemotherapy agents that control EGFR expression in cancer. Arsenic Trioxide 15-31 epidermal growth factor receptor Homo sapiens 43-47 34189121-5 2021 Interaction of Arsenic trioxide (ATO) with EGFR signalling pathway factors has been elicited by systematic search in data bases, as ATO is one of the mysterious chemotherapy agents that control EGFR expression in cancer. Arsenic Trioxide 15-31 epidermal growth factor receptor Homo sapiens 194-198 34189121-5 2021 Interaction of Arsenic trioxide (ATO) with EGFR signalling pathway factors has been elicited by systematic search in data bases, as ATO is one of the mysterious chemotherapy agents that control EGFR expression in cancer. Arsenic Trioxide 33-36 epidermal growth factor receptor Homo sapiens 43-47 34189121-5 2021 Interaction of Arsenic trioxide (ATO) with EGFR signalling pathway factors has been elicited by systematic search in data bases, as ATO is one of the mysterious chemotherapy agents that control EGFR expression in cancer. Arsenic Trioxide 33-36 epidermal growth factor receptor Homo sapiens 194-198 34189121-5 2021 Interaction of Arsenic trioxide (ATO) with EGFR signalling pathway factors has been elicited by systematic search in data bases, as ATO is one of the mysterious chemotherapy agents that control EGFR expression in cancer. Arsenic Trioxide 132-135 epidermal growth factor receptor Homo sapiens 43-47 34189121-5 2021 Interaction of Arsenic trioxide (ATO) with EGFR signalling pathway factors has been elicited by systematic search in data bases, as ATO is one of the mysterious chemotherapy agents that control EGFR expression in cancer. Arsenic Trioxide 132-135 epidermal growth factor receptor Homo sapiens 194-198 30237564-5 2018 In this study, arsenic trioxide (ATO) at 2 muM significantly inhibited the proliferation of the gefitinib-resistant NCI-H1975 cells of the EGFR L858R/T790M mutant compared with a modest inhibition in the gefitinib-sensitive HCC827 cells of DeltaE746-A750 mutant and A549 cells of wild-type EGFR. Arsenic Trioxide 15-31 epidermal growth factor receptor Homo sapiens 139-143 30237564-5 2018 In this study, arsenic trioxide (ATO) at 2 muM significantly inhibited the proliferation of the gefitinib-resistant NCI-H1975 cells of the EGFR L858R/T790M mutant compared with a modest inhibition in the gefitinib-sensitive HCC827 cells of DeltaE746-A750 mutant and A549 cells of wild-type EGFR. Arsenic Trioxide 15-31 epidermal growth factor receptor Homo sapiens 290-294 30237564-5 2018 In this study, arsenic trioxide (ATO) at 2 muM significantly inhibited the proliferation of the gefitinib-resistant NCI-H1975 cells of the EGFR L858R/T790M mutant compared with a modest inhibition in the gefitinib-sensitive HCC827 cells of DeltaE746-A750 mutant and A549 cells of wild-type EGFR. Arsenic Trioxide 33-36 epidermal growth factor receptor Homo sapiens 139-143 30237564-5 2018 In this study, arsenic trioxide (ATO) at 2 muM significantly inhibited the proliferation of the gefitinib-resistant NCI-H1975 cells of the EGFR L858R/T790M mutant compared with a modest inhibition in the gefitinib-sensitive HCC827 cells of DeltaE746-A750 mutant and A549 cells of wild-type EGFR. Arsenic Trioxide 33-36 epidermal growth factor receptor Homo sapiens 290-294 30237564-6 2018 Moreover, ATO significantly inhibited the overall kinase activity of EGFR primarily through quantitatively diminishing the EGFR in NCI-H1975 cells to an extent comparable with that reached by gefitinib in HCC827 cells. Arsenic Trioxide 10-13 epidermal growth factor receptor Homo sapiens 69-73 30237564-6 2018 Moreover, ATO significantly inhibited the overall kinase activity of EGFR primarily through quantitatively diminishing the EGFR in NCI-H1975 cells to an extent comparable with that reached by gefitinib in HCC827 cells. Arsenic Trioxide 10-13 epidermal growth factor receptor Homo sapiens 123-127 30237564-7 2018 Furthermore, ATO promoted autophagic degradation of EGFR in NSCLC cells by directly binding to P62, which interacted with EGFR, preferentially the L858R/T790M mutant providing a plausible explanation for a more favorable effect of ATO on NCI-H1975 cells. Arsenic Trioxide 13-16 epidermal growth factor receptor Homo sapiens 52-56 30237564-7 2018 Furthermore, ATO promoted autophagic degradation of EGFR in NSCLC cells by directly binding to P62, which interacted with EGFR, preferentially the L858R/T790M mutant providing a plausible explanation for a more favorable effect of ATO on NCI-H1975 cells. Arsenic Trioxide 13-16 epidermal growth factor receptor Homo sapiens 122-126 30237564-9 2018 Our results reveal a new target for ATO with a unique molecular mechanism, i.e., ATO suppresses the overall catalytic potential of EGFR, significantly those with the L858R/T790M mutant in NCI-H1975 cells, through an autophagic degradation by interacting with P62. Arsenic Trioxide 36-39 epidermal growth factor receptor Homo sapiens 131-135 30237564-9 2018 Our results reveal a new target for ATO with a unique molecular mechanism, i.e., ATO suppresses the overall catalytic potential of EGFR, significantly those with the L858R/T790M mutant in NCI-H1975 cells, through an autophagic degradation by interacting with P62. Arsenic Trioxide 81-84 epidermal growth factor receptor Homo sapiens 131-135 29274334-0 2018 Targeting of EGFR increase anti-cancer effects of arsenic trioxide: Promising treatment for glioblastoma multiform. Arsenic Trioxide 50-66 epidermal growth factor receptor Homo sapiens 13-17 29274334-5 2018 In this study, we use erlotinib as an EGFR inhibitor to increase the sensitivity of GBM cell lines to ATO treatment. Arsenic Trioxide 102-105 epidermal growth factor receptor Homo sapiens 38-42 29274334-12 2018 Present study uncovered that EGFR inhibition could overcome the resistance of glioblastoma cells to ATO treatment. Arsenic Trioxide 100-103 epidermal growth factor receptor Homo sapiens 29-33 25791921-10 2015 Therefore, we suggest that TGIF is transcriptionally regulated by the c-Src/EGFR/AKT pathway, which plays a role as a negative regulator in antagonizing ATO-induced CDKN1A expression and resultant apoptosis. Arsenic Trioxide 153-156 epidermal growth factor receptor Homo sapiens 76-80 23178716-7 2013 Collectively, As2O3 mediates an initial rise in pY-Src(416) to regulate the PI3K/AKT pathway which increases SnoN and cell survival; these early events may counter the cell death response associated with increased pY-EGFR/MAPK activation. Arsenic Trioxide 14-19 epidermal growth factor receptor Homo sapiens 217-221 23178716-3 2013 We now report that As2O3 increases phosphorylation of EGFR/p66ShcA and EGFR degradation. Arsenic Trioxide 19-24 epidermal growth factor receptor Homo sapiens 54-58 23548265-0 2013 Synergistic anticancer activity of arsenic trioxide with erlotinib is based on inhibition of EGFR-mediated DNA double-strand break repair. Arsenic Trioxide 35-51 epidermal growth factor receptor Homo sapiens 93-97 23548265-3 2013 Here, we show that inhibition of ATO-mediated EGF receptor (EGFR) activation can be used to potently sensitize diverse solid cancer types against ATO. Arsenic Trioxide 33-36 epidermal growth factor receptor Homo sapiens 46-58 23548265-3 2013 Here, we show that inhibition of ATO-mediated EGF receptor (EGFR) activation can be used to potently sensitize diverse solid cancer types against ATO. Arsenic Trioxide 33-36 epidermal growth factor receptor Homo sapiens 60-64 23548265-5 2013 Subsequent analyses revealed that this effect was based on the blockade of ATO-induced EGFR phosphorylation leading to more pronounced G2-M arrest as well as enhanced and more rapid induction of apoptosis. Arsenic Trioxide 75-78 epidermal growth factor receptor Homo sapiens 87-91 23548265-6 2013 Comparable ATO-sensitizing effects were also found with PI3K/AKT and mitogen-activated protein/extracellular signal-regulated kinase (MEK) inhibitors, suggesting an essential role of the EGFR-mediated downstream signaling pathway in cancer cell protection against ATO. Arsenic Trioxide 11-14 epidermal growth factor receptor Homo sapiens 187-191 23548265-6 2013 Comparable ATO-sensitizing effects were also found with PI3K/AKT and mitogen-activated protein/extracellular signal-regulated kinase (MEK) inhibitors, suggesting an essential role of the EGFR-mediated downstream signaling pathway in cancer cell protection against ATO. Arsenic Trioxide 264-267 epidermal growth factor receptor Homo sapiens 187-191 23548265-7 2013 H2AX staining and comet assay revealed that erlotinib significantly increases ATO-induced DNA double-strand breaks (DSB) well in accordance with a role of the EGFR signaling axis in DNA damage repair. Arsenic Trioxide 78-81 epidermal growth factor receptor Homo sapiens 159-163 23178716-3 2013 We now report that As2O3 increases phosphorylation of EGFR/p66ShcA and EGFR degradation. Arsenic Trioxide 19-24 epidermal growth factor receptor Homo sapiens 71-75 23178716-4 2013 As2O3 activates Src(Y416) whose activity (inhibited by PP2) modulates EGFR activation, its interaction with Shc/Grb2, and p-AKT. Arsenic Trioxide 0-5 epidermal growth factor receptor Homo sapiens 70-74 22532027-0 2012 NADPH oxidase-produced superoxide mediates EGFR transactivation by c-Src in arsenic trioxide-stimulated human keratinocytes. Arsenic Trioxide 76-92 epidermal growth factor receptor Homo sapiens 43-47 22532027-3 2012 Previously, we demonstrated in keratinocytes that arsenic trioxide (ATO)-induced p21(WAF1/CIP1) (p21) expression leading to cellular cytotoxicity through the c-Src/EGFR/ERK pathway and generation of reactive oxygen species (ROS). Arsenic Trioxide 50-66 epidermal growth factor receptor Homo sapiens 164-168 22532027-3 2012 Previously, we demonstrated in keratinocytes that arsenic trioxide (ATO)-induced p21(WAF1/CIP1) (p21) expression leading to cellular cytotoxicity through the c-Src/EGFR/ERK pathway and generation of reactive oxygen species (ROS). Arsenic Trioxide 68-71 epidermal growth factor receptor Homo sapiens 164-168 20435036-3 2010 Using arsenic trioxide-responsive KU7 and non-responsive 253JB-V bladder cancer cells as models, we show that in KU7 cells, < or =5 microM arsenic trioxide decreased Sp1, Sp3 and Sp4 and several Sp-dependent genes and responses including cyclin D1, epidermal growth factor receptor, bcl-2, survivin and vascular endothelial growth factor, whereas at concentrations up to 15 microM, minimal effects were observed in 253JB-V cells. Arsenic Trioxide 142-158 epidermal growth factor receptor Homo sapiens 252-284 15961274-0 2006 As2O3-induced c-Src/EGFR/ERK signaling is via Sp1 binding sites to stimulate p21WAF1/CIP1 expression in human epidermoid carcinoma A431 cells. Arsenic Trioxide 0-5 epidermal growth factor receptor Homo sapiens 20-24 22532027-10 2012 In addition, overexpression of c-Src as well as treatment with ATO could stimulate EGFR-Y845/ERK phosphorylation, p21 expression, and cellular arrest/apoptosis, which could be attenuated by pretreatment with apocynin or knockdown of p67(phox). Arsenic Trioxide 63-66 epidermal growth factor receptor Homo sapiens 83-87 21649584-11 2011 Collectively, we propose that the EGFR/PI3K/Akt pathway may regulate the post-transcriptional regulation of TGIF expression to antagonize ATO-induced apoptosis in HCC. Arsenic Trioxide 138-141 epidermal growth factor receptor Homo sapiens 34-38 15961274-4 2006 Using reporter assay, RT-PCR and Western blotting, we show that c-Src activation might be a prerequisite for As2O3-induced EGFR/Ras/Raf/ERK signaling. Arsenic Trioxide 109-114 epidermal growth factor receptor Homo sapiens 123-127 15961274-7 2006 Taken together, we conclude that the Sp1 binding sites are required for As2O3-induced p21 gene transcription through c-Src/EGFR/Ras/Raf/ERK pathway. Arsenic Trioxide 72-77 epidermal growth factor receptor Homo sapiens 123-127