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10.1038/srep16492 http://scihub22266oqcxt.onion/10.1038/srep16492 C4637930!4637930 !26549110     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26549110 &cmd=llinks): Failed to open stream: HTTP request failed! 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TIMP-1 mediates TGF-?-dependent crosstalk between hepatic stellate and cancer cells via FAK signaling |pdf=|usr=}}{{26549110 }} gab.com Text TIMP-1 mediates TGF- -dependent crosstalk between hepatic stellate and cancer cells via FAK signaling JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26549110 #FOAvip Transforming growth factor-? (TGF-?) signaling plays a key role in progression and metastasis of HCC. This study was undertaken to gain the proof of concept of a small-molecule inhibitor of TGF-? type I receptor kinase, EW-7197 as a potent anti-cancer therapy for HCC. We identified tissue inhibitors of metalloproteinases-1 (TIMP-1) as one of the secreted proteins of hepatic stellate cells (HSCs) and a key mediator of TGF-?-mediated crosstalk between HSCs and HCC cells. TGF-? signaling led to increased expression of TIMP-1, which activates focal adhesion kinase (FAK) signaling via its interaction with CD63. Inhibition of TGF-? signaling using EW-7197 significantly attenuated the progression and intrahepatic metastasis of HCC in an SK-HEP1-Luc orthotopic-xenograft mouse model. In addition, EW-7197 inhibited TGF-?-stimulated TIMP-1 secretion by HSCs as well as the TIMP-1-induced proliferation, motility, and survival of HCC cells. Further, EW-7197 interrupted TGF-?-mediated epithelial-to-mesenchymal transition and Akt signaling, leading to significant reductions in the motility and anchorage-independent growth of HCC cells. In conclusion, we found that TIMP-1 mediates TGF-?-regulated crosstalk between HSCs and HCC cells via FAK signaling. In addition, EW-7197 demonstrates potent in vivo anti-cancer therapeutic activity and may be a potential new anti-cancer drug of choice to treat patients with liver cancer. Twit Text FOAVip TIMP-1 mediates TGF- -dependent crosstalk between hepatic stellate and cancer cells via FAK signaling ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26549110 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26549110 #FOAvip English Wikipedia <ref>{{Cite pmid|26549110 }}</ref> TIMP-1 mediates TGF-?-dependent crosstalk between hepatic stellate and cancer cells via FAK signaling #MMPMID26549110 Park SA ; Kim MJ ; Park SY ; Kim JS ; Lim W ; Nam JS ; Yhong Sheen Y Sci Rep 2015[Nov]; 5 (ä): 16492 PMID26549110 show ga Transforming growth factor-? (TGF-?) signaling plays a key role in progression and metastasis of HCC. This study was undertaken to gain the proof of concept of a small-molecule inhibitor of TGF-? type I receptor kinase, EW-7197 as a potent anti-cancer therapy for HCC. We identified tissue inhibitors of metalloproteinases-1 (TIMP-1) as one of the secreted proteins of hepatic stellate cells (HSCs) and a key mediator of TGF-?-mediated crosstalk between HSCs and HCC cells. TGF-? signaling led to increased expression of TIMP-1, which activates focal adhesion kinase (FAK) signaling via its interaction with CD63. Inhibition of TGF-? signaling using EW-7197 significantly attenuated the progression and intrahepatic metastasis of HCC in an SK-HEP1-Luc orthotopic-xenograft mouse model. In addition, EW-7197 inhibited TGF-?-stimulated TIMP-1 secretion by HSCs as well as the TIMP-1-induced proliferation, motility, and survival of HCC cells. Further, EW-7197 interrupted TGF-?-mediated epithelial-to-mesenchymal transition and Akt signaling, leading to significant reductions in the motility and anchorage-independent growth of HCC cells. In conclusion, we found that TIMP-1 mediates TGF-?-regulated crosstalk between HSCs and HCC cells via FAK signaling. In addition, EW-7197 demonstrates potent in vivo anti-cancer therapeutic activity and may be a potential new anti-cancer drug of choice to treat patients with liver cancer. |*Cell Communication [MESH] |*Signal Transduction [MESH] |Aniline Compounds/pharmacology [MESH] |Animals [MESH] |Antineoplastic Agents/pharmacology [MESH] |Carcinoma, Hepatocellular/genetics/*metabolism/pathology [MESH] |Cell Line, Transformed [MESH] |Cell Line, Tumor [MESH] |Cell Movement/drug effects [MESH] |Cell Proliferation/drug effects [MESH] |Disease Models, Animal [MESH] |Disease Progression [MESH] |Epithelial-Mesenchymal Transition/drug effects [MESH] |Female [MESH] |Focal Adhesion Protein-Tyrosine Kinases/*metabolism [MESH] |Hepatic Stellate Cells/*metabolism [MESH] |Heterografts [MESH] |Humans [MESH] |Liver Neoplasms/genetics/*metabolism/pathology [MESH] |Mice [MESH] |Proto-Oncogene Proteins c-akt/metabolism [MESH] |Tissue Inhibitor of Metalloproteinase-1/*metabolism [MESH] |Transforming Growth Factor beta/antagonists & inhibitors/*metabolism [MESH]TIMP-1 mediates TGF-?-dependent crosstalk between hepatic stellate and(epmc).pdf DeepDyve Pubget Overpricing