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10.1111/cas.13157 http://scihub22266oqcxt.onion/10.1111/cas.13157 C5378260!5378260 !28064471     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28064471 &cmd=llinks): Failed to open stream: HTTP request failed! 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Vasohibin-2 is required for epithelial-mesenchymal transition of ovarian cancer cells by modulating transforming growth factor-? signaling |pdf=|usr=}}{{28064471 }} gab.com Text Vasohibin-2 is required for epithelial-mesenchymal transition of ovarian cancer cells by modulating transforming growth factor- signaling JO: Cancer Sci http://www.kidney.de/pget.php?&tw=1&pmid=28064471 #FOAvip Vasohibin-2 (VASH2) is a homolog of VASH1, an endothelium-derived angiogenesis inhibitor. Vasohibin-2 is mainly expressed in cancer cells, and has been implicated in the progression of cancer by inducing angiogenesis and tumor growth. Although VASH2 has been recently reported to be involved in epithelial-mesenchymal transition (EMT), its precise roles are obscure. The aim of the present study was to clarify the role of VASH2 in the EMT of cancer cells in relation to transforming growth factor-? (TGF-?) signaling, which is a major stimulator of EMT. Decreased expression of VASH2 in ovarian cancer cells significantly repressed the expression of TGF-? type I receptor, namely activin receptor-like kinase 5. Transforming growth factor-?1-induced phosphorylation of Smad2 and Smad3 was markedly decreased in VASH2 knockdown cells while the expression of Smad2 and Smad3 was unchanged. Accordingly, the responses to TGF-?1 shown by promoter assay and plasminogen activator inhibitor type 1 expression were significantly attenuated in VASH2 knockdown cells. Furthermore, knockdown of VASH2 in cancer cells abrogated the TGF-?1-induced reduced expression of epithelial markers including E-cadherin, and the elevated expression of mesenchymal markers including fibronectin, ZEB2, and Snail2, suggesting that endogenous VASH2 is required for TGF-?1-induced EMT. In accordance with these results, the effects of TGF-?1 on cell morphology, migration, invasion, and MMP2 expression were also abrogated when VASH2 was knocked down. These results indicate that VASH2 played a significant role in the EMT by modulating the TGF-? signaling. We propose that VASH2 would be a novel molecular target for the prevention of EMT in cancers. Twit Text FOAVip Vasohibin-2 is required for epithelial-mesenchymal transition of ovarian cancer cells by modulating transforming growth factor- signaling ????Cancer Sci http://www.kidney.de/pget.php?&tw=1&pmid=28064471 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28064471 #FOAvip English Wikipedia <ref>{{Cite pmid|28064471 }}</ref> Vasohibin-2 is required for epithelial-mesenchymal transition of ovarian cancer cells by modulating transforming growth factor-? signaling #MMPMID28064471 Norita R ; Suzuki Y ; Furutani Y ; Takahashi K ; Yoshimatsu Y ; Podyma-Inoue KA ; Watabe T ; Sato Y Cancer Sci 2017[Mar]; 108 (3 ): 419-426 PMID28064471 show ga Vasohibin-2 (VASH2) is a homolog of VASH1, an endothelium-derived angiogenesis inhibitor. Vasohibin-2 is mainly expressed in cancer cells, and has been implicated in the progression of cancer by inducing angiogenesis and tumor growth. Although VASH2 has been recently reported to be involved in epithelial-mesenchymal transition (EMT), its precise roles are obscure. The aim of the present study was to clarify the role of VASH2 in the EMT of cancer cells in relation to transforming growth factor-? (TGF-?) signaling, which is a major stimulator of EMT. Decreased expression of VASH2 in ovarian cancer cells significantly repressed the expression of TGF-? type I receptor, namely activin receptor-like kinase 5. Transforming growth factor-?1-induced phosphorylation of Smad2 and Smad3 was markedly decreased in VASH2 knockdown cells while the expression of Smad2 and Smad3 was unchanged. Accordingly, the responses to TGF-?1 shown by promoter assay and plasminogen activator inhibitor type 1 expression were significantly attenuated in VASH2 knockdown cells. Furthermore, knockdown of VASH2 in cancer cells abrogated the TGF-?1-induced reduced expression of epithelial markers including E-cadherin, and the elevated expression of mesenchymal markers including fibronectin, ZEB2, and Snail2, suggesting that endogenous VASH2 is required for TGF-?1-induced EMT. In accordance with these results, the effects of TGF-?1 on cell morphology, migration, invasion, and MMP2 expression were also abrogated when VASH2 was knocked down. These results indicate that VASH2 played a significant role in the EMT by modulating the TGF-? signaling. We propose that VASH2 would be a novel molecular target for the prevention of EMT in cancers. |Angiogenic Proteins/*genetics [MESH] |Cadherins/biosynthesis [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation/genetics [MESH] |Epithelial-Mesenchymal Transition/*genetics [MESH] |Female [MESH] |Fibronectins/biosynthesis [MESH] |Homeodomain Proteins/biosynthesis [MESH] |Humans [MESH] |Matrix Metalloproteinase 2/biosynthesis [MESH] |Neovascularization, Pathologic/genetics [MESH] |Ovarian Neoplasms/genetics/*pathology [MESH] |Phosphorylation/genetics [MESH] |Plasminogen Activator Inhibitor 1/biosynthesis [MESH] |Protein Serine-Threonine Kinases/biosynthesis [MESH] |RNA Interference [MESH] |RNA, Small Interfering/genetics [MESH] |Receptor, Transforming Growth Factor-beta Type I [MESH] |Receptors, Transforming Growth Factor beta/biosynthesis [MESH] |Repressor Proteins/biosynthesis [MESH] |Signal Transduction/*genetics [MESH] |Smad2 Protein/metabolism [MESH] |Smad3 Protein/metabolism [MESH] |Snail Family Transcription Factors/biosynthesis [MESH] |Transforming Growth Factor beta/*metabolism [MESH]Vasohibin-2 is required for epithelial-mesenchymal transition of ovari(epmc).pdf DeepDyve Pubget Overpricing