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10.18632/oncotarget.13373 http://scihub22266oqcxt.onion/10.18632/oncotarget.13373 C5348312!5348312 !27863394     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27863394 &cmd=llinks): Failed to open stream: HTTP request failed! 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MDA-9/Syntenin (SDCBP) modulates small GTPases RhoA and Cdc42 via transforming growth factor ?1 to enhance epithelial-mesenchymal transition in breast cancer |pdf=|usr=}}{{27863394 }} gab.com Text MDA-9/Syntenin (SDCBP) modulates small GTPases RhoA and Cdc42 via transforming growth factor 1 to enhance epithelial-mesenchymal transition in breast cancer JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27863394 #FOAvip Epithelial-mesenchymal transition (EMT) is one of the decisive steps regulating cancer invasion and metastasis. However, the molecular mechanisms underlying this transition require further clarification. MDA-9/syntenin (SDCBP) expression is elevated in breast cancer patient samples as well as cultured breast cancer cells. Silencing expression of MDA-9 in mesenchymal metastatic breast cancer cells triggered a change in cell morphology in both 2D- and 3D-cultures to a more epithelial-like phenotype, along with changes in EMT markers, cytoskeletal rearrangement and decreased invasion. Conversely, over expressing MDA-9 in epithelial non-metastatic breast cancer cells instigated a change in morphology to a more mesenchymal phenotype with corresponding changes in EMT markers, cytoskeletal rearrangement and an increase in invasion. We also found that MDA-9 upregulated active levels of known modulators of EMT, the small GTPases RhoA and Cdc42, via TGF?1. Reintroducing TGF?1 in MDA-9 silenced cells restored active RhoA and cdc42 levels, modulated cytoskeletal rearrangement and increased invasion. We further determined that MDA-9 interacts with TGF?1 via its PDZ1 domain. Finally, in vivo studies demonstrated that silencing the expression of MDA-9 resulted in decreased lung metastasis and TGF?1 re-expression partially restored lung metastases. Our findings provide evidence for the relevance of MDA-9 in mediating EMT in breast cancer and support the potential of MDA-9 as a therapeutic target against metastatic disease. Twit Text FOAVip MDA-9/Syntenin (SDCBP) modulates small GTPases RhoA and Cdc42 via transforming growth factor 1 to enhance epithelial-mesenchymal transition in breast cancer ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27863394 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27863394 #FOAvip English Wikipedia <ref>{{Cite pmid|27863394 }}</ref> MDA-9/Syntenin (SDCBP) modulates small GTPases RhoA and Cdc42 via transforming growth factor ?1 to enhance epithelial-mesenchymal transition in breast cancer #MMPMID27863394 Menezes ME ; Shen XN ; Das SK ; Emdad L ; Sarkar D ; Fisher PB Oncotarget 2016[Dec]; 7 (49 ): 80175-80189 PMID27863394 show ga Epithelial-mesenchymal transition (EMT) is one of the decisive steps regulating cancer invasion and metastasis. However, the molecular mechanisms underlying this transition require further clarification. MDA-9/syntenin (SDCBP) expression is elevated in breast cancer patient samples as well as cultured breast cancer cells. Silencing expression of MDA-9 in mesenchymal metastatic breast cancer cells triggered a change in cell morphology in both 2D- and 3D-cultures to a more epithelial-like phenotype, along with changes in EMT markers, cytoskeletal rearrangement and decreased invasion. Conversely, over expressing MDA-9 in epithelial non-metastatic breast cancer cells instigated a change in morphology to a more mesenchymal phenotype with corresponding changes in EMT markers, cytoskeletal rearrangement and an increase in invasion. We also found that MDA-9 upregulated active levels of known modulators of EMT, the small GTPases RhoA and Cdc42, via TGF?1. Reintroducing TGF?1 in MDA-9 silenced cells restored active RhoA and cdc42 levels, modulated cytoskeletal rearrangement and increased invasion. We further determined that MDA-9 interacts with TGF?1 via its PDZ1 domain. Finally, in vivo studies demonstrated that silencing the expression of MDA-9 resulted in decreased lung metastasis and TGF?1 re-expression partially restored lung metastases. Our findings provide evidence for the relevance of MDA-9 in mediating EMT in breast cancer and support the potential of MDA-9 as a therapeutic target against metastatic disease. |*Epithelial-Mesenchymal Transition [MESH] |Actin Cytoskeleton/enzymology/pathology [MESH] |Animals [MESH] |Breast Neoplasms/*enzymology/genetics/pathology [MESH] |Cell Line, Tumor [MESH] |Cell Movement [MESH] |Cell Shape [MESH] |Female [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Humans [MESH] |Lung Neoplasms/enzymology/genetics/secondary [MESH] |Mice, Nude [MESH] |Neoplasm Invasiveness [MESH] |Phenotype [MESH] |Protein Interaction Domains and Motifs [MESH] |RNA Interference [MESH] |Signal Transduction [MESH] |Syntenins/genetics/*metabolism [MESH] |Time Factors [MESH] |Transfection [MESH] |Transforming Growth Factor beta1/genetics/*metabolism [MESH] |cdc42 GTP-Binding Protein/genetics/*metabolism [MESH]MDA-9/Syntenin (SDCBP) modulates small GTPases RhoA and Cdc42 via tran(epmc).pdf DeepDyve Pubget Overpricing