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10.3892/or.2016.5338 http://scihub22266oqcxt.onion/10.3892/or.2016.5338 C5355686!5355686 !28035402     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28035402 &cmd=llinks): Failed to open stream: HTTP request failed! 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Transforming growth factor-?1 suppresses bone morphogenetic protein-2-induced mesenchymal-epithelial transition in HSC-4 human oral squamous cell carcinoma cells via Smad1/5/9 pathway suppression |pdf=|usr=}}{{28035402 }} gab.com Text Transforming growth factor- 1 suppresses bone morphogenetic protein-2-induced mesenchymal-epithelial transition in HSC-4 human oral squamous cell carcinoma cells via Smad1/5/9 pathway suppression JO: Oncol Rep http://www.kidney.de/pget.php?&tw=1&pmid=28035402 #FOAvip Squamous cell carcinoma is the most common cancer in the oral cavity. We previously demonstrated that transforming growth factor-?1 (TGF-?1) promotes the epithelial-mesenchymal transition (EMT) of human oral squamous cell carcinoma (hOSCC) cells; however, it remains to be clarified whether the TGF-? superfamily member bone morphogenetic protein (BMP) affects this process in hOSCC cells. Here, we examined the independent and collective effects of TGF-?1 and BMP-2 on EMT and mesenchymal?epithelial transition (MET) in a panel of four hOSCC cell lines. Notably, we found that HSC-4 cells were the most responsive to BMP-2 stimulation, which resulted in the upregulation of Smad1/5/9 target genes such as the MET inducers ID1 and cytokeratin 9 (CK9). Furthermore, BMP-2 downregulated the mesenchymal marker N-cadherin and the EMT inducer Snail, but upregulated epithelial CK9 expression, indicating that BMP-2 prefers to induce MET rather than EMT. Moreover, TGF-?1 dampened BMP-2-induced epithelial gene expression by inhibiting Smad1/5/9 expression and phosphorylation. Functional analysis revealed that TGF-?1 and BMP-2 significantly enhanced HSC-4 cell migration and proliferation, respectively. Collectively, these data suggest that TGF-? positively regulates hOSCC invasion in the primary tumor, whereas BMP-2 facilitates cancer cell colonization at secondary metastatic sites. Thus, the invasive and metastatic characteristics of hOSCC appear to be reciprocally regulated by BMP and TGF-?. Twit Text FOAVip Transforming growth factor- 1 suppresses bone morphogenetic protein-2-induced mesenchymal-epithelial transition in HSC-4 human oral squamous cell carcinoma cells via Smad1/5/9 pathway suppression ????Oncol Rep http://www.kidney.de/pget.php?&tw=1&pmid=28035402 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28035402 #FOAvip English Wikipedia <ref>{{Cite pmid|28035402 }}</ref> Transforming growth factor-?1 suppresses bone morphogenetic protein-2-induced mesenchymal-epithelial transition in HSC-4 human oral squamous cell carcinoma cells via Smad1/5/9 pathway suppression #MMPMID28035402 Chiba T ; Ishisaki A ; Kyakumoto S ; Shibata T ; Yamada H ; Kamo M Oncol Rep 2017[Feb]; 37 (2 ): 713-720 PMID28035402 show ga Squamous cell carcinoma is the most common cancer in the oral cavity. We previously demonstrated that transforming growth factor-?1 (TGF-?1) promotes the epithelial-mesenchymal transition (EMT) of human oral squamous cell carcinoma (hOSCC) cells; however, it remains to be clarified whether the TGF-? superfamily member bone morphogenetic protein (BMP) affects this process in hOSCC cells. Here, we examined the independent and collective effects of TGF-?1 and BMP-2 on EMT and mesenchymal?epithelial transition (MET) in a panel of four hOSCC cell lines. Notably, we found that HSC-4 cells were the most responsive to BMP-2 stimulation, which resulted in the upregulation of Smad1/5/9 target genes such as the MET inducers ID1 and cytokeratin 9 (CK9). Furthermore, BMP-2 downregulated the mesenchymal marker N-cadherin and the EMT inducer Snail, but upregulated epithelial CK9 expression, indicating that BMP-2 prefers to induce MET rather than EMT. Moreover, TGF-?1 dampened BMP-2-induced epithelial gene expression by inhibiting Smad1/5/9 expression and phosphorylation. Functional analysis revealed that TGF-?1 and BMP-2 significantly enhanced HSC-4 cell migration and proliferation, respectively. Collectively, these data suggest that TGF-? positively regulates hOSCC invasion in the primary tumor, whereas BMP-2 facilitates cancer cell colonization at secondary metastatic sites. Thus, the invasive and metastatic characteristics of hOSCC appear to be reciprocally regulated by BMP and TGF-?. |Apoptosis/drug effects [MESH] |Blotting, Western [MESH] |Bone Morphogenetic Protein 2/*pharmacology [MESH] |Carcinoma, Squamous Cell/drug therapy/genetics/metabolism/*pathology [MESH] |Cell Movement/drug effects [MESH] |Cell Proliferation/drug effects [MESH] |Epithelial-Mesenchymal Transition/*drug effects [MESH] |Gene Expression Regulation, Neoplastic/*drug effects [MESH] |Humans [MESH] |Mouth Neoplasms/drug therapy/genetics/metabolism/*pathology [MESH] |RNA, Messenger/genetics [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |Smad Proteins/genetics/*metabolism [MESH] |Smad1 Protein/genetics/metabolism [MESH] |Smad5 Protein/genetics/metabolism [MESH] |Smad8 Protein/genetics/metabolism [MESH] |Transforming Growth Factor beta1/*pharmacology [MESH]Transforming growth factor-?1 suppresses bone morphogenetic protein-2-(epmc).pdf DeepDyve Pubget Overpricing