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10.18632/oncotarget.8047 http://scihub22266oqcxt.onion/10.18632/oncotarget.8047 C5008391!5008391 !26993767     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 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\26993767 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Oncotarget 2016 ; 7 (16 ): 22674-86 Nephropedia Template TP {{tp|p=26993767 |t=2016. MicroRNA-630 suppresses tumor metastasis through the TGF-?- miR-630-Slug signaling pathway and correlates inversely with poor prognosis in hepatocellular carcinoma |pdf=|usr=}}{{26993767 }} gab.com Text MicroRNA-630 suppresses tumor metastasis through the TGF- - miR-630-Slug signaling pathway and correlates inversely with poor prognosis in hepatocellular carcinoma JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26993767 #FOAvip The epithelial-mesenchymal transition (EMT) is the key process that drives tumor metastasis. Accumulating evidence suggests that the deregulation of some microRNAs (miRNAs), is implicated in this process. Here, we highlight the function and molecular mechanism of miR-630 and its potential clinical application in hepatocellular carcinoma (HCC). First, we identified the clinical relevance of miR-630 expression in a screen of 97 HCC patient tissues. Patients with low miR-630 expression had higher recurrence rates and shorter overall survival than those with high miR-630 expression. Functional studies demonstrated the overexpression of miR-630 in HCC cells attenuated the EMT phenotype in vitro. Conversely, inhibition of miR-630 promoted EMT in HCC cells. Mechanistically, our data revealed that miR-630 suppressed EMT by targeting Slug. Knockdown of Slug expression reversed miR-630 inhibitor-mediated EMT progression. Furthermore, we found that the TGF-?-Erk/SP1 and JNK/c-Jun signaling pathways repressed miR-630 transcription through occupying transcription factor binding sites. Ectopic expression of miR-630 restored the TGF-?-activated EMT process. Taken together, these findings demonstrate, in HCC cells, miR-630 exerts its tumor-suppressor functions through the TGF-?-miR-630-Slug axis and provides a potential prognostic predictor for HCC patients. Twit Text FOAVip MicroRNA-630 suppresses tumor metastasis through the TGF- - miR-630-Slug signaling pathway and correlates inversely with poor prognosis in hepatocellular carcinoma ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26993767 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26993767 #FOAvip English Wikipedia <ref>{{Cite pmid|26993767 }}</ref> MicroRNA-630 suppresses tumor metastasis through the TGF-?- miR-630-Slug signaling pathway and correlates inversely with poor prognosis in hepatocellular carcinoma #MMPMID26993767 Chen WX ; Zhang ZG ; Ding ZY ; Liang HF ; Song J ; Tan XL ; Wu JJ ; Li GZ ; Zeng Z ; Zhang BX ; Chen XP Oncotarget 2016[Apr]; 7 (16 ): 22674-86 PMID26993767 show ga The epithelial-mesenchymal transition (EMT) is the key process that drives tumor metastasis. Accumulating evidence suggests that the deregulation of some microRNAs (miRNAs), is implicated in this process. Here, we highlight the function and molecular mechanism of miR-630 and its potential clinical application in hepatocellular carcinoma (HCC). First, we identified the clinical relevance of miR-630 expression in a screen of 97 HCC patient tissues. Patients with low miR-630 expression had higher recurrence rates and shorter overall survival than those with high miR-630 expression. Functional studies demonstrated the overexpression of miR-630 in HCC cells attenuated the EMT phenotype in vitro. Conversely, inhibition of miR-630 promoted EMT in HCC cells. Mechanistically, our data revealed that miR-630 suppressed EMT by targeting Slug. Knockdown of Slug expression reversed miR-630 inhibitor-mediated EMT progression. Furthermore, we found that the TGF-?-Erk/SP1 and JNK/c-Jun signaling pathways repressed miR-630 transcription through occupying transcription factor binding sites. Ectopic expression of miR-630 restored the TGF-?-activated EMT process. Taken together, these findings demonstrate, in HCC cells, miR-630 exerts its tumor-suppressor functions through the TGF-?-miR-630-Slug axis and provides a potential prognostic predictor for HCC patients. |Animals [MESH] |Biomarkers, Tumor/analysis [MESH] |Carcinoma, Hepatocellular/genetics/mortality/*pathology [MESH] |Epithelial-Mesenchymal Transition/genetics [MESH] |Female [MESH] |Gene Expression Regulation, Neoplastic/*genetics [MESH] |Heterografts [MESH] |Humans [MESH] |Kaplan-Meier Estimate [MESH] |Liver Neoplasms/genetics/mortality/*pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Nude [MESH] |MicroRNAs/genetics/*metabolism [MESH] |Neoplasm Invasiveness/genetics/pathology [MESH] |Prognosis [MESH] |Signal Transduction/genetics [MESH]MicroRNA-630 suppresses tumor metastasis through the TGF-?- miR-630-Sl(epmc).pdf DeepDyve Pubget Overpricing