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http://scihub22266oqcxt.onion/ C5384991!5384991!28401017     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Cancer+Res 2017 ; 7 (3): 628-46 Nephropedia Template TP {{tp|p=28401017|t=2017. miR-495 promotes the chemoresistance of SCLC through the epithelial-mesenchymal transition via Etk/BMX |pdf=|usr=}}{{28401017}} gab.com Text miR-495 promotes the chemoresistance of SCLC through the epithelial-mesenchymal transition via Etk/BMX JO: Am J Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=28401017 #FOAvip miR-495 serves as an oncogenic miRNA or a tumor suppressor in different types of cancer. However, its role in the drug resistance of small cell lung cancer (SCLC) remains unidentified. In this study, we investigated whether miR-495 regulates the chemoresistance of SCLC through the epithelial-mesenchymal transition (EMT) via Epithelial and endothelial tyrosine kinase (Etk/BMX) using two drug-resistant cell lines. Loss- and gain-of-function experiments showed miR-495 regulated cell proliferation, tumor growth and drug resistance. miR-495 suppression or Etk/BMX elevation in SCLC specimens was correlated with poor pathologic stage and survival time. Etk/BMX was one of the directly targeted genes of miR-495. Ectopic expression of Etk/BMX obviously rescued the miR-495 elevation elevation-induced inhibition of drug resistance. Etk/BMX over-expression led to higher levels of EMT mesenchymal factors (Zeb-2, Twist, Vim) and lower levels of the epithelial molecule ?-catenin, while suppression of Etk/BMX showed the opposite trend. Knockdown of Zeb-2 and Twist inhibited the chemoresistance of cells. Our study revealed that miR-495 promoted the chemoresistance of SCLC through the epithelial-mesenchymal transition via Etk/BMX. miR-495 re-expression or Etk/BMX depletion is a promising strategy for interfering with chemoresistance in SCLC. Twit Text FOAVip miR-495 promotes the chemoresistance of SCLC through the epithelial-mesenchymal transition via Etk/BMX ????Am J Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=28401017 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28401017 #FOAvip English Wikipedia <ref>{{Cite pmid|28401017}}</ref> miR-495 promotes the chemoresistance of SCLC through the epithelial-mesenchymal transition via Etk/BMX #MMPMID28401017 Wei T; Zhu W; Fang S; Zeng X; Huang J; Yang J; Zhang J; Guo L Am J Cancer Res 2017[]; 7 (3): 628-46 PMID28401017show ga miR-495 serves as an oncogenic miRNA or a tumor suppressor in different types of cancer. However, its role in the drug resistance of small cell lung cancer (SCLC) remains unidentified. In this study, we investigated whether miR-495 regulates the chemoresistance of SCLC through the epithelial-mesenchymal transition (EMT) via Epithelial and endothelial tyrosine kinase (Etk/BMX) using two drug-resistant cell lines. Loss- and gain-of-function experiments showed miR-495 regulated cell proliferation, tumor growth and drug resistance. miR-495 suppression or Etk/BMX elevation in SCLC specimens was correlated with poor pathologic stage and survival time. Etk/BMX was one of the directly targeted genes of miR-495. Ectopic expression of Etk/BMX obviously rescued the miR-495 elevation elevation-induced inhibition of drug resistance. Etk/BMX over-expression led to higher levels of EMT mesenchymal factors (Zeb-2, Twist, Vim) and lower levels of the epithelial molecule ?-catenin, while suppression of Etk/BMX showed the opposite trend. Knockdown of Zeb-2 and Twist inhibited the chemoresistance of cells. Our study revealed that miR-495 promoted the chemoresistance of SCLC through the epithelial-mesenchymal transition via Etk/BMX. miR-495 re-expression or Etk/BMX depletion is a promising strategy for interfering with chemoresistance in SCLC. ämiR-495 promotes the chemoresistance of SCLC through the epithelial-me(epmc).pdf DeepDyve Pubget Overpricing