PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33921192-6 2021 Western blot assay demonstrated that resveratrol combined with cisplatin significantly reduced the expression of fibronectin, vimentin, P-AKT, P-PI3K, P-JNK, P-ERK, Sma2, and Smad3 induced by TGF-beta1 (p < 0.05), and increased the expression of E-cadherin (p < 0.05), respectively. Cisplatin 63-72 cadherin 1 Homo sapiens 246-256 29798292-5 2018 Western blot assay show the protein expression of Snail and MDR1 were down-regulated in transfected Hep-2/CDDP cells (allP<0.05), while epithelial marker E-cadherin was up-regulated in protein level (P<0.05).Conclusion:Small interference of transcription factor Snail could increase the expression of E-cadherin while decrease the expression of MDR1, and it was confirmed that interference Snail contribute to enhanced cisplatin sensitivity on human laryngeal resistant cancer cells. Cisplatin 425-434 cadherin 1 Homo sapiens 157-167 31320606-0 2019 Correction: 3-deazaneplanocin A protects against cisplatin-induced renal tubular cell apoptosis and acute kidney injury by restoration of E-cadherin expression. Cisplatin 49-58 cadherin 1 Homo sapiens 138-148 31186697-1 2019 The aim of the present study was to assess the expression of epithelial-mesenchymal transition biomarkers (E-cadherin and vimentin) and their potential significance as prognostic markers in patients with stage IIIB/IV non-squamous non-small cell lung cancer (NSCLC) enrolled in the INNOVATIONS trial, receiving treatment with either erlotinib/bevacizumab (EB) or cisplatin/gemcitabine/bevacizumab (PGB). Cisplatin 363-372 cadherin 1 Homo sapiens 107-117 31024010-12 2019 These data suggest that PAX6 can mediate E-cadherin downregulation through the PI3K/AKT signaling pathway by directly binding the promoter region of ZEB2, thereby mediating cell migration, stem cell transformation, and cisplatin resistance; and ultimately, affecting survival in NSCLC patients. Cisplatin 219-228 cadherin 1 Homo sapiens 41-51 29767234-4 2018 Importantly, miR-125a-5p enhanced the cytotoxic effects of cisplatin on EC1 and TE1 cells, and co-treatment with miR-125a-5p and cisplatin significantly induced cell apoptosis and reduced the cell migratory and invasive abilities of EC1 and TE1 cells, coupled with an increase in the E-cadherin level and a decrease in the N-cadherin and Vimentin levels. Cisplatin 59-68 cadherin 1 Homo sapiens 284-294 29767234-4 2018 Importantly, miR-125a-5p enhanced the cytotoxic effects of cisplatin on EC1 and TE1 cells, and co-treatment with miR-125a-5p and cisplatin significantly induced cell apoptosis and reduced the cell migratory and invasive abilities of EC1 and TE1 cells, coupled with an increase in the E-cadherin level and a decrease in the N-cadherin and Vimentin levels. Cisplatin 129-138 cadherin 1 Homo sapiens 284-294 29928330-6 2018 Furthermore, LSD1 knockdown plus cisplatin synergistically impaired cell migration via the induction of the epithelial marker E-cadherin and inhibition of the mesenchymal markers, snail family transcriptional repressor 1 and Vimentin. Cisplatin 33-42 cadherin 1 Homo sapiens 126-136 32710593-8 2020 CONCLUSION: Nanog directly participated in the regulation of Slug, E-cadherin, Oct-4, and c-Myc genes, causing cisplatin resistance/recurrence of OSCC. Cisplatin 111-120 cadherin 1 Homo sapiens 67-77 32734935-8 2020 Moreover, cur C086+cisplatin suppressed BMIL1 expression or its potential downstream targets, P16, E-cadherin, EGFR, and Notch1. Cisplatin 19-28 cadherin 1 Homo sapiens 99-109 31066485-10 2019 CDH1 (encoding the epithelial cell marker E-cadherin) and IL2RA (encoding the Treg marker CD25) expression in patients with stage IV lung cancer that were resistant to cisplatin treatment showed an inverse correlation between IL2RA (high) and CDH1 (low) expression. Cisplatin 168-177 cadherin 1 Homo sapiens 0-4 31066485-10 2019 CDH1 (encoding the epithelial cell marker E-cadherin) and IL2RA (encoding the Treg marker CD25) expression in patients with stage IV lung cancer that were resistant to cisplatin treatment showed an inverse correlation between IL2RA (high) and CDH1 (low) expression. Cisplatin 168-177 cadherin 1 Homo sapiens 243-247 31043583-7 2019 In contrast, 3-DZNeP treatment potentiated the cytotoxic effect of cisplatin in H1299, a non-small cell lung cancer cell line that expresses lower E-cadherin levels. Cisplatin 67-76 cadherin 1 Homo sapiens 147-157 30653577-13 2019 We found that cisplatin-resistant cell line A2780cis cells differ from their cisplatin-sensitive counterparts in the CDH1 methylation. Cisplatin 14-23 cadherin 1 Homo sapiens 117-121 30653577-13 2019 We found that cisplatin-resistant cell line A2780cis cells differ from their cisplatin-sensitive counterparts in the CDH1 methylation. Cisplatin 77-86 cadherin 1 Homo sapiens 117-121 29996940-11 2018 Accordingly, 3D cultures of E-cadherin-expressing EOC cells are sensitive to the CDK5 inhibitor roscovitine combined with cisplatin. Cisplatin 122-131 cadherin 1 Homo sapiens 28-38 25008268-6 2014 Although the suspension cell masses of all three cell lines were proliferatively stagnant, possibly due to cell cycle arrest at G1/S, cell mortality at 72 h after cisplatin treatment was significantly decreased in the high E-cadherin SKOV-3 cells compared to SKOV-3 cells without E-cadherin expression and to OVCAR-3 cells with low E-cadherin expression. Cisplatin 163-172 cadherin 1 Homo sapiens 223-233 29163683-3 2017 A previous study by the authors of the present study demonstrated that HMGN5 contributes to the progression of urothelial bladder cancer (UBC) through regulating the expression of E-cadherin and vascular endothelial growth factor (VEGF)-C, which are associated with the sensitivity of tumor cells to cisplatin. Cisplatin 300-309 cadherin 1 Homo sapiens 180-190 28053596-8 2017 RESULTS: MDR1, MRP1, BCRP and Trkb, E-cadherin, beta-catenin were significantly downregulated in cells treated with the combination of celecoxib and cisplatin, and decreased beta-catenin level was found in cells with wortmannin, a specific PI3K inhibitor. Cisplatin 149-158 cadherin 1 Homo sapiens 36-46 30091550-6 2016 Compared with Arisaematis Rhizoma polysaccharide group and cisplatin group, there were higher in the early,late apoptosis rate and E-cadherin mRNA levels, lower the mRNA levels of Vimentin, N-cadherin, FN and p-Akt / Akt in combined group( P <0. Cisplatin 59-68 cadherin 1 Homo sapiens 131-141 29358506-8 2018 Mechanistic studies demonstrated that cisplatin treatment induced phosphorylation of AKT and loss of E-cadherin in the nephrotoxic kidney, and administration of TA enhanced AKT phosphorylation and preserved E-cadherin expression. Cisplatin 38-47 cadherin 1 Homo sapiens 101-111 29515788-3 2018 CD44s induced an EMT phenotype in cisplatin resistant cells by up-regulating ZEB1, a transcriptional repressor of E-cadherin. Cisplatin 34-43 cadherin 1 Homo sapiens 114-124 28212573-6 2017 SLFN11 and E-cadherin were also significantly associated with in vitro sensitivity to cisplatin and topoisomerase1/2 inhibitors (all commonly used in SCLC). Cisplatin 86-95 cadherin 1 Homo sapiens 11-21 28212573-7 2017 Treatment with cisplatin or PARP inhibitors downregulated SLFN11 and E-cadherin, possibly explaining the rapid development of therapeutic resistance in SCLC. Cisplatin 15-24 cadherin 1 Homo sapiens 69-79 27186392-0 2016 MicroRNA-10b regulates epithelial-mesenchymal transition by modulating KLF4/Notch1/E-cadherin in cisplatin-resistant nasopharyngeal carcinoma cells. Cisplatin 97-106 cadherin 1 Homo sapiens 83-93 24935589-0 2014 Cisplatin combined with metformin inhibits migration and invasion of human nasopharyngeal carcinoma cells by regulating E-cadherin and MMP-9. Cisplatin 0-9 cadherin 1 Homo sapiens 120-130 21618587-4 2011 We demonstrate that cisplatin-induced transition from epithelial to mesenchymal morphology in residual cancer cells correlated with reduced E-cadherin, and increased N-cadherin and vimentin expression. Cisplatin 20-29 cadherin 1 Homo sapiens 140-150 21519793-7 2011 ENTPD6 expression was involved in cellular sensitivity to cisplatin through an interaction with E-cadherin. Cisplatin 58-67 cadherin 1 Homo sapiens 96-106 14985455-4 2004 In so doing, we found that disruption of E-cadherin-mediated adhesion sensitizes multicellular spheroids of HT29 in vitro to treatment with 5-fluorouracil, paclitaxel, vinblastine, and etoposide but not cisplatin. Cisplatin 203-212 cadherin 1 Homo sapiens 41-51 17959171-0 2008 Deletion of exon 8 increases cisplatin-induced E-cadherin cleavage. Cisplatin 29-38 cadherin 1 Homo sapiens 47-57 17959171-3 2008 Here, we analysed the fate of E-cadherin with an in frame deletion of exon 8 compared to wild-type E-cadherin and the involved signalling events during cisplatin-induced apoptosis. Cisplatin 152-161 cadherin 1 Homo sapiens 30-40 17959171-9 2008 In summary, we clearly demonstrate that somatic E-cadherin mutations affect apoptosis regulation in that way that they can facilitate the disruption of adherens junctions thereby possibly influencing the response to cisplatin-based chemotherapy. Cisplatin 216-225 cadherin 1 Homo sapiens 48-58 19584296-6 2009 Independent validation experiment using five new pancreatic cancer cell lines confirmed that an inverse correlation between E-cadherin and Zeb-1 correlated closely with resistance to gemcitabine, 5-FU, and cisplatin. Cisplatin 206-215 cadherin 1 Homo sapiens 124-134 16244579-4 2005 RESULTS: It has been shown that the formation of the resistance to cisplatin in A2780/DDP8 cells is accompanied by the increase of expression of glutathione-S-transferase and Bcl-2, by the decrease of expression of CD95-antigene and proliferation potential of the cells, by appearance of EGF receptors and elevation of expression level of E-cadherin, alpha- and beta-catenins, proving the enhancement of adhesive properties of tumor cells. Cisplatin 67-76 cadherin 1 Homo sapiens 339-349 15138368-0 2004 Effect of wild-type and mutant E-cadherin on cell proliferation and responsiveness to the chemotherapeutic agents cisplatin, etoposide, and 5-fluorouracil. Cisplatin 114-123 cadherin 1 Homo sapiens 31-41 15138368-2 2004 The aim of the present study was to investigate the impact of wild-type (wt) E-cadherin and tumor-derived mutant E-cadherin variants on the proliferation rate of MDA-MB-435S mammary carcinoma cells and the sensitivity of the cells to the chemotherapeutic drugs cisplatin, etoposide and 5-fluorouracil (5-FU) and whether p53 is involved in the chemotherapeutic response. Cisplatin 261-270 cadherin 1 Homo sapiens 113-123 15138368-9 2004 Cisplatin sensitivity of wt and mutant E-cadherin-expressing MDA-MB-435S cells was reduced as compared with E-cadherin-negative, parental MDA-MB-435S cells. Cisplatin 0-9 cadherin 1 Homo sapiens 39-49 15138368-9 2004 Cisplatin sensitivity of wt and mutant E-cadherin-expressing MDA-MB-435S cells was reduced as compared with E-cadherin-negative, parental MDA-MB-435S cells. Cisplatin 0-9 cadherin 1 Homo sapiens 108-118 35443865-9 2022 Our study suggested that IRF6 may enhance chemotherapeutic sensitivity of cisplatin mediated by affecting cell proliferation, migration and invasion along with apoptosis through regulating E-cadherin and Ki67, while the identified molecular mechanisms remain to be further explored. Cisplatin 74-83 cadherin 1 Homo sapiens 189-199 33478150-5 2021 We showed that expression of SNAIL1 and N-cadherin are the highest in cisplatin-resistant A2780cis and SK-OV-3 cells, while high SNAIL2 and E-cadherin levels were observed in cisplatin-sensitive A2780 cells. Cisplatin 175-184 cadherin 1 Homo sapiens 140-150 34360933-7 2021 Our results showed that a cisplatin/cetuximab combination treatment inhibited cell proliferation, cell motility, and N-cadherin protein expression but induced E-cadherin and claudin-1 protein expression. Cisplatin 26-35 cadherin 1 Homo sapiens 159-169