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10.1038/cddis.2017.114 http://scihub22266oqcxt.onion/10.1038/cddis.2017.114 C5520876!5520876!28569772     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28569772&cmd=llinks): Failed to open stream: HTTP request failed! 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Deficiency of pigment epithelium-derived factor in nasopharyngeal carcinoma cells triggers the epithelial?mesenchymal transition and metastasis |pdf=|usr=}}{{28569772}} gab.com Text Deficiency of pigment epithelium-derived factor in nasopharyngeal carcinoma cells triggers the epithelial mesenchymal transition and metastasis JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28569772 #FOAvip Distant metastasis is the primary cause of nasopharyngeal carcinoma (NPC) treatment failure while epithelial?mesenchymal transition (EMT) is the critical process of NPC invasion and metastasis. However, tumor-suppressor genes involved in the EMT and metastasis of NPC have not been explored clearly compared with the oncogenes. In the present study, the expression of pigment epithelium-derived factor (PEDF), a potent endogenous antitumor factor, was diminished in human NPC tissues and associated with clinicopathological and EMT features. The knockdown of PEDF induced EMT in lower metastatic NPC cell lines and overexpression of PEDF restored epithelial phenotype in higher metastatic NPC cell lines with typical EMT. The inhibition of PEDF mediated NPC cell spontaneous metastasis in vivo. LRP6/GSK3?/?-catenin signal pathway rather than AKT/GSK3? pathway was involved in the effects of PEDF on EMT. The expression of PEDF was directly downregulated by elevated miR-320c in NPC. In conclusion, our findings indicate for the first time that PEDF functions as tumor-suppressor gene in the occurrence of EMT and metastasis in NPC. PEDF could serve as a promising candidate for NPC diagnosis, prognosis and treatment. Twit Text FOAVip Deficiency of pigment epithelium-derived factor in nasopharyngeal carcinoma cells triggers the epithelial mesenchymal transition and metastasis ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28569772 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28569772 #FOAvip English Wikipedia <ref>{{Cite pmid|28569772}}</ref> Deficiency of pigment epithelium-derived factor in nasopharyngeal carcinoma cells triggers the epithelial?mesenchymal transition and metastasis #MMPMID28569772 Zhang T; Yin P; Zhang Z; Xu B; Che D; Dai Z; Dong C; Jiang P; Hong H; Yang Z; Zhou T; Shao J; Xu Z; Yang X; Gao G Cell Death Dis 2017[Jun]; 8 (6): e2838- PMID28569772show ga Distant metastasis is the primary cause of nasopharyngeal carcinoma (NPC) treatment failure while epithelial?mesenchymal transition (EMT) is the critical process of NPC invasion and metastasis. However, tumor-suppressor genes involved in the EMT and metastasis of NPC have not been explored clearly compared with the oncogenes. In the present study, the expression of pigment epithelium-derived factor (PEDF), a potent endogenous antitumor factor, was diminished in human NPC tissues and associated with clinicopathological and EMT features. The knockdown of PEDF induced EMT in lower metastatic NPC cell lines and overexpression of PEDF restored epithelial phenotype in higher metastatic NPC cell lines with typical EMT. The inhibition of PEDF mediated NPC cell spontaneous metastasis in vivo. LRP6/GSK3?/?-catenin signal pathway rather than AKT/GSK3? pathway was involved in the effects of PEDF on EMT. The expression of PEDF was directly downregulated by elevated miR-320c in NPC. In conclusion, our findings indicate for the first time that PEDF functions as tumor-suppressor gene in the occurrence of EMT and metastasis in NPC. PEDF could serve as a promising candidate for NPC diagnosis, prognosis and treatment. äDeficiency of pigment epithelium-derived factor in nasopharyngeal carc(epmc).pdf DeepDyve Pubget Overpricing