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Down-regulated FSTL5 promotes cell proliferation and survival by affecting Wnt/?-catenin signaling in hepatocellular carcinoma |pdf=|usr=}}{{26045876}} gab.com Text Down-regulated FSTL5 promotes cell proliferation and survival by affecting Wnt/ -catenin signaling in hepatocellular carcinoma JO: Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26045876 #FOAvip Follistatin-like 5 (FSTL5), a member of the follistatin family of genes, encodes a secretory glycoprotein. Previous study revealed that it might play a suppressive role in hepatocellular carcinoma (HCC). However, its clinical significances, biological functions and molecular mechanisms in HCC development are poorly understood. To gain insight to the functions of FSTL5 in HCC, We examined FSTL5 expression pattern in 117 HCC tissue samples. The results of immunohistochemical staining analysis showed that FSTL5 is more commonly down-regulated in HCC compared to adjacent tissues and further clinicopathological analysis showed that its expression level is closely correlated with tumor size, TNM stage, local infiltration and patient prognosis. Both gain function assays and recombinant human FSTL5 protein treatment assays in vitro revealed that over-expressing FSTL5 could inhibit the abilities of cancer cell proliferation and survival. Further, we found that those effects on HCC growth and survival are associated with Wnt/?-catenin signaling. Taken together, all of our results validate that FSTL5 plays a suppressive role in HCC and suggest that down-regulated FSTL5 could elevate abilities of growth and survival of HCC cells by activation of Wnt/?-catenin signaling. Twit Text FOAVip Down-regulated FSTL5 promotes cell proliferation and survival by affecting Wnt/ -catenin signaling in hepatocellular carcinoma ????Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26045876 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26045876 #FOAvip English Wikipedia <ref>{{Cite pmid|26045876}}</ref> Down-regulated FSTL5 promotes cell proliferation and survival by affecting Wnt/?-catenin signaling in hepatocellular carcinoma #MMPMID26045876 Zhang D; Ma X; Sun W; Cui P; Lu Z Int J Clin Exp Pathol 2015[]; 8 (3): 3386-94 PMID26045876show ga Follistatin-like 5 (FSTL5), a member of the follistatin family of genes, encodes a secretory glycoprotein. Previous study revealed that it might play a suppressive role in hepatocellular carcinoma (HCC). However, its clinical significances, biological functions and molecular mechanisms in HCC development are poorly understood. To gain insight to the functions of FSTL5 in HCC, We examined FSTL5 expression pattern in 117 HCC tissue samples. The results of immunohistochemical staining analysis showed that FSTL5 is more commonly down-regulated in HCC compared to adjacent tissues and further clinicopathological analysis showed that its expression level is closely correlated with tumor size, TNM stage, local infiltration and patient prognosis. Both gain function assays and recombinant human FSTL5 protein treatment assays in vitro revealed that over-expressing FSTL5 could inhibit the abilities of cancer cell proliferation and survival. Further, we found that those effects on HCC growth and survival are associated with Wnt/?-catenin signaling. Taken together, all of our results validate that FSTL5 plays a suppressive role in HCC and suggest that down-regulated FSTL5 could elevate abilities of growth and survival of HCC cells by activation of Wnt/?-catenin signaling. äDown-regulated FSTL5 promotes cell proliferation and survival by affec(epmc).pdf DeepDyve Pubget Overpricing