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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! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2016 ; 7 (16): 21315-31 Nephropedia Template TP {{tp|p=26824324|t=2016. 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 PMID26824324show 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. äMetformin inhibits 17?-estradiol-induced epithelial-to-mesenchymal tra(epmc).pdf DeepDyve Pubget Overpricing