Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

http://scihub22266oqcxt.onion/ C4673297!4673297!26023734     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2015 ; 6 (25): 21704-17 Nephropedia Template TP {{tp|p=26023734|t=2015. ER? inhibits epithelial-mesenchymal transition by suppressing Bmi1 in breast cancer |pdf=|usr=}}{{26023734}} gab.com Text ER inhibits epithelial-mesenchymal transition by suppressing Bmi1 in breast cancer JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26023734 #FOAvip In human breast cancer, estrogen receptor-? (ER?) suppresses epithelial-mesenchymal transition (EMT) and stemness, two crucial parameters for tumor metastasis; however, the underlying mechanism by which ER? regulates these two processes remains largely unknown. Bmi1, the polycomb group protein B lymphoma Mo-MLV insertion region 1 homolog, regulates EMT transition, maintains the self-renewal capacity of stem cells, and is frequently overexpressed in human cancers. In the present study, ER? upregulated the expression of the epithelial marker, E-cadherin, in breast cancer cells through the transcriptional down-regulation of Bmi1. Furthermore, ER? overexpression suppressed the migration, invasion, and EMT of breast cancer cells. Notably, overexpression of ER? significantly decreased the CD44high/CD24low cell population and inhibited the capacity for mammosphere formation in ER?-negative breast cancer cells. In addition, overexpression of Bmi1 attenuated the ER?-mediated suppression of EMT and cell stemness. Immunohistochemistry revealed an inverse association of ER? and Bmi1 expression in human breast cancer tissue. Taken together, our findings suggest that ER? inhibits EMT and stemness through the downregulation of Bmi1. Twit Text FOAVip ER inhibits epithelial-mesenchymal transition by suppressing Bmi1 in breast cancer ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26023734 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26023734 #FOAvip English Wikipedia <ref>{{Cite pmid|26023734}}</ref> ER? inhibits epithelial-mesenchymal transition by suppressing Bmi1 in breast cancer #MMPMID26023734 Wei XL; Dou XW; Bai JW; Luo XR; Qiu SQ; Xi DD; Huang WH; Du CW; Man K; Zhang GJ Oncotarget 2015[Aug]; 6 (25): 21704-17 PMID26023734show ga In human breast cancer, estrogen receptor-? (ER?) suppresses epithelial-mesenchymal transition (EMT) and stemness, two crucial parameters for tumor metastasis; however, the underlying mechanism by which ER? regulates these two processes remains largely unknown. Bmi1, the polycomb group protein B lymphoma Mo-MLV insertion region 1 homolog, regulates EMT transition, maintains the self-renewal capacity of stem cells, and is frequently overexpressed in human cancers. In the present study, ER? upregulated the expression of the epithelial marker, E-cadherin, in breast cancer cells through the transcriptional down-regulation of Bmi1. Furthermore, ER? overexpression suppressed the migration, invasion, and EMT of breast cancer cells. Notably, overexpression of ER? significantly decreased the CD44high/CD24low cell population and inhibited the capacity for mammosphere formation in ER?-negative breast cancer cells. In addition, overexpression of Bmi1 attenuated the ER?-mediated suppression of EMT and cell stemness. Immunohistochemistry revealed an inverse association of ER? and Bmi1 expression in human breast cancer tissue. Taken together, our findings suggest that ER? inhibits EMT and stemness through the downregulation of Bmi1. äER? inhibits epithelial-mesenchymal transition by suppressing Bmi1 in (epmc).pdf DeepDyve Pubget Overpricing