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10.1038/bjc.2017.164 http://scihub22266oqcxt.onion/10.1038/bjc.2017.164 C5520514!5520514!28588321     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 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28588321.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Br+J+Cancer 2017 ; 117 (2): 233-44 Nephropedia Template TP {{tp|p=28588321|t=2017. MicroRNA-199b-5p attenuates TGF-?1-induced epithelial?mesenchymal transition in hepatocellular carcinoma |pdf=|usr=}}{{28588321}} gab.com Text MicroRNA-199b-5p attenuates TGF- 1-induced epithelial mesenchymal transition in hepatocellular carcinoma JO: Br J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28588321 #FOAvip Background:: Accumulating evidence indicates that N-cadherin is a cell adhesion molecule that has critical roles in tumour progression. However, the role of N-cadherin in hepatocellular carcinoma (HCC) remains controversial. Methods:: This study aims to investigate the expression status of N-cadherin and its molecular mechanisms in HCC. Results:: The expression of N-cadherin was markedly overexpressed in HCC tissues and cell lines. We identified that miR-199b-5p binds to the 3?-UTR of N-cadherin mRNA, thus decreasing N-cadherin expression in HCC cells. We also found the downregulation of miR-199b-5p in HCC specimens, which was inversely correlated with N-cadherin upregulation, predicted poor clinical outcomes in HCC patients. Next, we determined that miR-199b-5p overexpression promoted cell aggregation, suppressed cell migration and invasion in HCC cells, and inhibited xenografts tumour metastasis in nude mice. Moreover, we demonstrated that miR-199b-5p attenuated TGF-?1 induced epithelial?mesenchymal transition (EMT) -associated traits, while its effects could be partially reversed by N-cadherin restoration. Finally, we examined that N-cadherin downregulation or miR-199b-5p overexpression suppressed TGF-?1-induced Akt phosphorylation, and inhibition of PI3K/Akt pathway blocked TGF-?1-induced N-cadherin overexpression in HCC cells. Conclusions:: Our data demonstrate that N-Cadherin was markedly overexpressed and miR-199b-5p was significantly downregulated in HCC. MiR-199b-5p exerts inhibitory effects on EMT, and directly targets N-cadherin in HCC, supporting the potential utility of miR-199b-5p as a promising strategy to treat HCC. Also, a positive regulatory loop exists between N-cadherin and Akt signalling represents a novel mechanism of TGF-?1-mediated EMT in HCC cells. Twit Text FOAVip MicroRNA-199b-5p attenuates TGF- 1-induced epithelial mesenchymal transition in hepatocellular carcinoma ????Br J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28588321 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28588321 #FOAvip English Wikipedia <ref>{{Cite pmid|28588321}}</ref> MicroRNA-199b-5p attenuates TGF-?1-induced epithelial?mesenchymal transition in hepatocellular carcinoma #MMPMID28588321 Zhou Sj; Liu Fy; Zhang Ah; Liang Hf; Wang Y; Ma R; Jiang Yh; Sun Nf Br J Cancer 2017[Jul]; 117 (2): 233-44 PMID28588321show ga Background:: Accumulating evidence indicates that N-cadherin is a cell adhesion molecule that has critical roles in tumour progression. However, the role of N-cadherin in hepatocellular carcinoma (HCC) remains controversial. Methods:: This study aims to investigate the expression status of N-cadherin and its molecular mechanisms in HCC. Results:: The expression of N-cadherin was markedly overexpressed in HCC tissues and cell lines. We identified that miR-199b-5p binds to the 3?-UTR of N-cadherin mRNA, thus decreasing N-cadherin expression in HCC cells. We also found the downregulation of miR-199b-5p in HCC specimens, which was inversely correlated with N-cadherin upregulation, predicted poor clinical outcomes in HCC patients. Next, we determined that miR-199b-5p overexpression promoted cell aggregation, suppressed cell migration and invasion in HCC cells, and inhibited xenografts tumour metastasis in nude mice. Moreover, we demonstrated that miR-199b-5p attenuated TGF-?1 induced epithelial?mesenchymal transition (EMT) -associated traits, while its effects could be partially reversed by N-cadherin restoration. Finally, we examined that N-cadherin downregulation or miR-199b-5p overexpression suppressed TGF-?1-induced Akt phosphorylation, and inhibition of PI3K/Akt pathway blocked TGF-?1-induced N-cadherin overexpression in HCC cells. Conclusions:: Our data demonstrate that N-Cadherin was markedly overexpressed and miR-199b-5p was significantly downregulated in HCC. MiR-199b-5p exerts inhibitory effects on EMT, and directly targets N-cadherin in HCC, supporting the potential utility of miR-199b-5p as a promising strategy to treat HCC. Also, a positive regulatory loop exists between N-cadherin and Akt signalling represents a novel mechanism of TGF-?1-mediated EMT in HCC cells. �MicroRNA-199b-5p attenuates TGF-?1-induced epithelial?mesenchymal tran(epmc).pdf DeepDyve Pubget Overpricing