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10.18632/oncotarget.3023 http://scihub22266oqcxt.onion/10.18632/oncotarget.3023 C4467113!4467113 !25749031     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25749031 &cmd=llinks): Failed to open stream: HTTP request failed! 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FAK activation is required for IGF1R-mediated regulation of EMT, migration, and invasion in mesenchymal triple negative breast cancer cells |pdf=|usr=}}{{25749031 }} gab.com Text FAK activation is required for IGF1R-mediated regulation of EMT, migration, and invasion in mesenchymal triple negative breast cancer cells JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=25749031 #FOAvip Triple negative breast cancer (TNBC) is a highly metastatic disease that currently lacks effective prevention and treatment strategies. The insulin-like growth factor 1 receptor (IGF1R) and focal adhesion kinase (FAK) signaling pathways function in numerous developmental processes, and alterations in both are linked with a number of common pathological diseases. Overexpression of IGF1R and FAK are closely associated with metastatic breast tumors. The present study investigated the interrelationship between IGF1R and FAK signaling in regulating the malignant properties of TNBC cells. Using small hairpin RNA (shRNA)-mediated IGF1R silencing methods, we showed that IGF1R is essential for sustaining mesenchymal morphologies of TNBC cells and modulates the expression of EMT-related markers. We further showed that IGF1R overexpression promotes migratory and invasive behaviors of TNBC cell lines. Most importantly, IGF1R-driven migration and invasion is predominantly mediated by FAK activation and can be suppressed using pharmacological inhibitors of FAK. Our findings in TNBC cells demonstrate a novel role of the IGF1R/FAK signaling pathway in regulating critical processes involved in the metastatic cascade. These results may improve the current understanding of the basic molecular mechanisms of TNBC metastasis and provide a strong rationale for co-targeting of IGF1R and FAK as therapy for mesenchymal TNBCs. Twit Text FOAVip FAK activation is required for IGF1R-mediated regulation of EMT, migration, and invasion in mesenchymal triple negative breast cancer cells ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=25749031 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25749031 #FOAvip English Wikipedia <ref>{{Cite pmid|25749031 }}</ref> FAK activation is required for IGF1R-mediated regulation of EMT, migration, and invasion in mesenchymal triple negative breast cancer cells #MMPMID25749031 Taliaferro-Smith L ; Oberlick E ; Liu T ; McGlothen T ; Alcaide T ; Tobin R ; Donnelly S ; Commander R ; Kline E ; Nagaraju GP ; Havel L ; Marcus A ; Nahta R ; O'Regan R Oncotarget 2015[Mar]; 6 (7 ): 4757-72 PMID25749031 show ga Triple negative breast cancer (TNBC) is a highly metastatic disease that currently lacks effective prevention and treatment strategies. The insulin-like growth factor 1 receptor (IGF1R) and focal adhesion kinase (FAK) signaling pathways function in numerous developmental processes, and alterations in both are linked with a number of common pathological diseases. Overexpression of IGF1R and FAK are closely associated with metastatic breast tumors. The present study investigated the interrelationship between IGF1R and FAK signaling in regulating the malignant properties of TNBC cells. Using small hairpin RNA (shRNA)-mediated IGF1R silencing methods, we showed that IGF1R is essential for sustaining mesenchymal morphologies of TNBC cells and modulates the expression of EMT-related markers. We further showed that IGF1R overexpression promotes migratory and invasive behaviors of TNBC cell lines. Most importantly, IGF1R-driven migration and invasion is predominantly mediated by FAK activation and can be suppressed using pharmacological inhibitors of FAK. Our findings in TNBC cells demonstrate a novel role of the IGF1R/FAK signaling pathway in regulating critical processes involved in the metastatic cascade. These results may improve the current understanding of the basic molecular mechanisms of TNBC metastasis and provide a strong rationale for co-targeting of IGF1R and FAK as therapy for mesenchymal TNBCs. |*Cell Movement [MESH] |*Cell Proliferation [MESH] |*Epithelial-Mesenchymal Transition [MESH] |Apoptosis [MESH] |Blotting, Western [MESH] |Female [MESH] |Focal Adhesion Kinase 1/antagonists & inhibitors/genetics/*metabolism [MESH] |Humans [MESH] |Immunoenzyme Techniques [MESH] |Mesenchymal Stem Cells/metabolism/*pathology [MESH] |RNA, Messenger/genetics [MESH] |RNA, Small Interfering/genetics [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Receptor, IGF Type 1/genetics/*metabolism [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |Triple Negative Breast Neoplasms/genetics/metabolism/*pathology [MESH]FAK activation is required for IGF1R-mediated regulation of EMT, migra(epmc).pdf DeepDyve Pubget Overpricing