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10.1186/s13046-018-0773-8 http://scihub22266oqcxt.onion/10.1186/s13046-018-0773-8 C5948853!5948853 !29751820     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29751820 &cmd=llinks): Failed to open stream: HTTP request failed! 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Physical interaction of STAT1 isoforms with TGF-? receptors leads to functional crosstalk between two signaling pathways in epithelial ovarian cancer |pdf=|usr=}}{{29751820 }} gab.com Text Physical interaction of STAT1 isoforms with TGF- receptors leads to functional crosstalk between two signaling pathways in epithelial ovarian cancer JO: J Exp Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=29751820 #FOAvip BACKGROUND: The signal transducer and activator of transcription (STAT) and transforming growth factor-? (TGF-?) signaling pathways play important roles in epithelial ovarian cancer (EOC). However, the mechanism of crosstalk between two pathways is not completely understood. METHODS: The expression of STAT1 protein was detected by tissue microarray and immunoblotting (IB). The interaction of STAT1 isoforms with TGF-? receptors was confirmed by immunoprecipitation and IB. The effect of TGF-? signaling on STAT1 activation was examined in EOC and non-tumorous HOSEpiC cells treated with TGF-?1 in the presence or absence of the inhibitor of TGF-? type I receptor. The gain-of-function and loss-of-function approaches were applied for detecting the role of STAT1 on EOC cell behaviours. RESULTS: The high level of STAT1 was observed in patients with high-grade serous EOC. STAT1 expression was higher in ovarian cancer cells than noncancerous cells. TGF-?1 activated the STAT1 pathway by inducing the phosphorylation of STAT1? on S727 residue. The full-length STAT1? and the truncated STAT1? directly interacted with TGF-? receptors (ALK1/ALK5 and T?RII), which was mediated by TGF-?1. STAT1? and STAT1? blocked the activation of the TGF-?1 signaling pathway in EOC cells by reducing Smad2 phosphorylation. STAT1 overexpression induced EOC cell proliferation, migration, and invasion; whereas its inhibition enhanced TGF-?1-induced phospho-Smad2 and suppressed EOC cell proliferation, migration, and invasion. CONCLUSIONS: Our data unveil a novel insight into the molecular mechanism of crosstalk between the STAT1 and TGF-? signaling pathways, which affected the cancer cell behavior. Suppression of STAT1 may be a potential therapeutic strategy for targeting ovarian cancer. Twit Text FOAVip Physical interaction of STAT1 isoforms with TGF- receptors leads to functional crosstalk between two signaling pathways in epithelial ovarian cancer ????J Exp Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=29751820 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29751820 #FOAvip English Wikipedia <ref>{{Cite pmid|29751820 }}</ref> Physical interaction of STAT1 isoforms with TGF-? receptors leads to functional crosstalk between two signaling pathways in epithelial ovarian cancer #MMPMID29751820 Tian X ; Guan W ; Zhang L ; Sun W ; Zhou D ; Lin Q ; Ren W ; Nadeem L ; Xu G J Exp Clin Cancer Res 2018[May]; 37 (1 ): 103 PMID29751820 show ga BACKGROUND: The signal transducer and activator of transcription (STAT) and transforming growth factor-? (TGF-?) signaling pathways play important roles in epithelial ovarian cancer (EOC). However, the mechanism of crosstalk between two pathways is not completely understood. METHODS: The expression of STAT1 protein was detected by tissue microarray and immunoblotting (IB). The interaction of STAT1 isoforms with TGF-? receptors was confirmed by immunoprecipitation and IB. The effect of TGF-? signaling on STAT1 activation was examined in EOC and non-tumorous HOSEpiC cells treated with TGF-?1 in the presence or absence of the inhibitor of TGF-? type I receptor. The gain-of-function and loss-of-function approaches were applied for detecting the role of STAT1 on EOC cell behaviours. RESULTS: The high level of STAT1 was observed in patients with high-grade serous EOC. STAT1 expression was higher in ovarian cancer cells than noncancerous cells. TGF-?1 activated the STAT1 pathway by inducing the phosphorylation of STAT1? on S727 residue. The full-length STAT1? and the truncated STAT1? directly interacted with TGF-? receptors (ALK1/ALK5 and T?RII), which was mediated by TGF-?1. STAT1? and STAT1? blocked the activation of the TGF-?1 signaling pathway in EOC cells by reducing Smad2 phosphorylation. STAT1 overexpression induced EOC cell proliferation, migration, and invasion; whereas its inhibition enhanced TGF-?1-induced phospho-Smad2 and suppressed EOC cell proliferation, migration, and invasion. CONCLUSIONS: Our data unveil a novel insight into the molecular mechanism of crosstalk between the STAT1 and TGF-? signaling pathways, which affected the cancer cell behavior. Suppression of STAT1 may be a potential therapeutic strategy for targeting ovarian cancer. |*Signal Transduction [MESH] |Biomarkers [MESH] |Carcinoma, Ovarian Epithelial/genetics/*metabolism/pathology [MESH] |Cell Line, Tumor [MESH] |Cell Movement [MESH] |Cell Proliferation [MESH] |Cell Transformation, Neoplastic [MESH] |Female [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Humans [MESH] |Neoplasm Grading [MESH] |Neoplasm Staging [MESH] |Protein Binding [MESH] |Protein Isoforms [MESH] |RNA, Small Interfering [MESH] |Receptors, Transforming Growth Factor beta/*metabolism [MESH] |STAT1 Transcription Factor/*metabolism [MESH]Physical interaction of STAT1 isoforms with TGF-? receptors leads to f(epmc).pdf DeepDyve Pubget Overpricing