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10.18632/oncotarget.7040 http://scihub22266oqcxt.onion/10.18632/oncotarget.7040 C5008287!5008287 !26824324     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26824324 &cmd=llinks): Failed to open stream: HTTP request failed! 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Metformin inhibits 17?-estradiol-induced epithelial-to-mesenchymal transition via ?Klotho-related ERK1/2 signaling and AMPK? signaling in endometrial adenocarcinoma cells |pdf=|usr=}}{{26824324 }} gab.com Text Metformin inhibits 17 -estradiol-induced epithelial-to-mesenchymal transition via Klotho-related ERK1/2 signaling and AMPK signaling in endometrial adenocarcinoma cells JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26824324 #FOAvip The potential role of metformin in treating endometrial cancer remains to be explored. The current study investigated the role of metformin in 17?-estradiol-induced epithelial-mesenchymal transition (EMT) in endometrial adenocarcinoma cells. We found that 17?-estradiol promoted proliferation and migration, attenuated apoptosis in both estrogen receptor (ER) positive and ER negative endometrial adenocarcinoma cells (Ishikawa and KLE cells, respectively). Metformin abolished 17?-estradiol-induced cell proliferation and reversed 17?-estradiol-induced EMT in Ishikawa cells. In addition, metformin increased the expression of ?Klotho, a fibroblast growth factors (FGFs) coreceptor, and decreased ERK1/2 phosphorylation in both Ishikawa and KLE cells. Decreased expression of ?Klotho was noted in human endometrial adenocarcinomas, and plasmid-driven expression of ?Klotho in Ishikawa cells abolished 17?-estradiol-induced EMT via inhibiting ERK1/2 signaling. ?Klotho expression and metformin show synergetic effects on the proliferation and the EMT in Ishikawa cells. Furthermore, we demonstrated that the anti-EMT effects of metformin could be partly abolished by introducing Compound C, a specific AMPK? signaling inhibitor. In conclusion, metformin abolishes 17?-estradiol-induced cell proliferation and EMT in endometrial adenocarcinoma cells by upregulating ?Klotho expression, inhibiting ERK1/2 signaling, and activating AMPK? signaling. Our study provides novel mechanistic insight into the anti-tumor effects of metformin. Twit Text FOAVip Metformin inhibits 17 -estradiol-induced epithelial-to-mesenchymal transition via Klotho-related ERK1/2 signaling and AMPK signaling in endometrial adenocarcinoma cells ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26824324 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26824324 #FOAvip English Wikipedia <ref>{{Cite pmid|26824324 }}</ref> Metformin inhibits 17?-estradiol-induced epithelial-to-mesenchymal transition via ?Klotho-related ERK1/2 signaling and AMPK? signaling in endometrial adenocarcinoma cells #MMPMID26824324 Liu Z ; Qi S ; Zhao X ; Li M ; Ding S ; Lu J ; Zhang H Oncotarget 2016[Apr]; 7 (16 ): 21315-31 PMID26824324 show ga The potential role of metformin in treating endometrial cancer remains to be explored. The current study investigated the role of metformin in 17?-estradiol-induced epithelial-mesenchymal transition (EMT) in endometrial adenocarcinoma cells. We found that 17?-estradiol promoted proliferation and migration, attenuated apoptosis in both estrogen receptor (ER) positive and ER negative endometrial adenocarcinoma cells (Ishikawa and KLE cells, respectively). Metformin abolished 17?-estradiol-induced cell proliferation and reversed 17?-estradiol-induced EMT in Ishikawa cells. In addition, metformin increased the expression of ?Klotho, a fibroblast growth factors (FGFs) coreceptor, and decreased ERK1/2 phosphorylation in both Ishikawa and KLE cells. Decreased expression of ?Klotho was noted in human endometrial adenocarcinomas, and plasmid-driven expression of ?Klotho in Ishikawa cells abolished 17?-estradiol-induced EMT via inhibiting ERK1/2 signaling. ?Klotho expression and metformin show synergetic effects on the proliferation and the EMT in Ishikawa cells. Furthermore, we demonstrated that the anti-EMT effects of metformin could be partly abolished by introducing Compound C, a specific AMPK? signaling inhibitor. In conclusion, metformin abolishes 17?-estradiol-induced cell proliferation and EMT in endometrial adenocarcinoma cells by upregulating ?Klotho expression, inhibiting ERK1/2 signaling, and activating AMPK? signaling. Our study provides novel mechanistic insight into the anti-tumor effects of metformin. |AMP-Activated Protein Kinases/metabolism [MESH] |Adenocarcinoma/*drug therapy/metabolism/pathology [MESH] |Adult [MESH] |Apoptosis [MESH] |Biomarkers, Tumor/*metabolism [MESH] |Cell Movement [MESH] |Cell Proliferation [MESH] |Endometrial Neoplasms/*drug therapy/metabolism/pathology [MESH] |Endometrium/drug effects/metabolism/pathology [MESH] |Epithelial-Mesenchymal Transition/*drug effects [MESH] |Estradiol/*pharmacology [MESH] |Estrogens/pharmacology [MESH] |Female [MESH] |Gene Expression Regulation, Neoplastic/*drug effects [MESH] |Humans [MESH] |Hypoglycemic Agents/pharmacology [MESH] |Klotho Proteins [MESH] |Membrane Proteins/metabolism [MESH] |Metformin/*pharmacology [MESH] |Middle Aged [MESH] |Mitogen-Activated Protein Kinase 1/metabolism [MESH] |Mitogen-Activated Protein Kinase 3/metabolism [MESH] |Phosphorylation [MESH] |Receptors, Estrogen/metabolism [MESH] |Signal Transduction [MESH]Metformin inhibits 17?-estradiol-induced epithelial-to-mesenchymal tra(epmc).pdf DeepDyve Pubget Overpricing