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10.3390/cancers7020822 http://scihub22266oqcxt.onion/10.3390/cancers7020822 C4491697!4491697!26083935     free     free     free Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancers+(Basel) 2015 ; 7 (2): 1022-36 Nephropedia Template TP {{tp|p=26083935|t=2015. Involvement of 14-3-3 Proteins in Regulating Tumor Progression of Hepatocellular Carcinoma |pdf=|usr=}}{{26083935}} gab.com Text Involvement of 14-3-3 Proteins in Regulating Tumor Progression of Hepatocellular Carcinoma JO: Cancers (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=26083935 #FOAvip There are seven mammalian isoforms of the 14-3-3 protein, which regulate multiple cellular functions via interactions with phosphorylated partners. Increased expression of 14-3-3 proteins contributes to tumor progression of various malignancies. Several isoforms of 14-3-3 are overexpressed and associate with higher metastatic risks and poorer survival rates of hepatocellular carcinoma (HCC). 14-3-3? and 14-3-3? regulate HCC cell proliferation, tumor growth and chemosensitivity via modulating mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK) and p38 signal pathways. Moreover, 14-3-3? suppresses E-cadherin and induces focal adhesion kinase (FAK) expression, thereby enhancing epithelial-mesenchymal transition (EMT) and HCC cell migration. 14-3-3? forms complexes with ?B-crystallin, which induces EMT and is the cause of sorafenib resistance in HCC. Finally, a recent study has indicated that 14-3-3? induces heat shock protein 70 (HSP70) expression, which increases HCC cell migration. These results suggest that selective 14-3-3 isoforms contribute to cell proliferation, EMT and cell migration of HCC by regulating distinct targets and signal pathways. Targeting 14-3-3 proteins together with specific downstream effectors therefore has potential to be therapeutic and prognostic factors of HCC. In this article, we will overview 14-3-3?s regulation of its downstream factors and contributions to HCC EMT, cell migration and proliferation. Twit Text FOAVip Involvement of 14-3-3 Proteins in Regulating Tumor Progression of Hepatocellular Carcinoma ????Cancers (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=26083935 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26083935 #FOAvip English Wikipedia <ref>{{Cite pmid|26083935}}</ref> Involvement of 14-3-3 Proteins in Regulating Tumor Progression of Hepatocellular Carcinoma #MMPMID26083935 Wu YJ; Jan YJ; Ko BS; Liang SM; Liou JY Cancers (Basel) 2015[Jun]; 7 (2): 1022-36 PMID26083935show ga There are seven mammalian isoforms of the 14-3-3 protein, which regulate multiple cellular functions via interactions with phosphorylated partners. Increased expression of 14-3-3 proteins contributes to tumor progression of various malignancies. Several isoforms of 14-3-3 are overexpressed and associate with higher metastatic risks and poorer survival rates of hepatocellular carcinoma (HCC). 14-3-3? and 14-3-3? regulate HCC cell proliferation, tumor growth and chemosensitivity via modulating mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK) and p38 signal pathways. Moreover, 14-3-3? suppresses E-cadherin and induces focal adhesion kinase (FAK) expression, thereby enhancing epithelial-mesenchymal transition (EMT) and HCC cell migration. 14-3-3? forms complexes with ?B-crystallin, which induces EMT and is the cause of sorafenib resistance in HCC. Finally, a recent study has indicated that 14-3-3? induces heat shock protein 70 (HSP70) expression, which increases HCC cell migration. These results suggest that selective 14-3-3 isoforms contribute to cell proliferation, EMT and cell migration of HCC by regulating distinct targets and signal pathways. Targeting 14-3-3 proteins together with specific downstream effectors therefore has potential to be therapeutic and prognostic factors of HCC. In this article, we will overview 14-3-3?s regulation of its downstream factors and contributions to HCC EMT, cell migration and proliferation. äInvolvement of 14-3-3 Proteins in Regulating Tumor Progression of Hepa(epmc).pdf DeepDyve Pubget Overpricing