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10.1242/jcs.180539 http://scihub22266oqcxt.onion/10.1242/jcs.180539 C4878991!4878991 !27076520     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27076520 &cmd=llinks): Failed to open stream: HTTP request failed! 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Mechanical signals regulate and activate SNAIL1 protein to control the fibrogenic response of cancer-associated fibroblasts |pdf=|usr=}}{{27076520 }} gab.com Text Mechanical signals regulate and activate SNAIL1 protein to control the fibrogenic response of cancer-associated fibroblasts JO: J Cell Sci http://www.kidney.de/pget.php?&tw=1&pmid=27076520 #FOAvip Increased deposition of collagen in extracellular matrix (ECM) leads to increased tissue stiffness and occurs in breast tumors. When present, this increases tumor invasion and metastasis. Precisely how this deposition is regulated and maintained in tumors is unclear. Much has been learnt about mechanical signal transduction in cells, but transcriptional responses and the pathophysiological consequences are just becoming appreciated. Here, we show that the SNAIL1 (also known as SNAI1) protein level increases and accumulates in nuclei of breast tumor cells and cancer-associated fibroblasts (CAFs) following exposure to stiff ECM in culture and in vivo SNAIL1 is required for the fibrogenic response of CAFs when exposed to a stiff matrix. ECM stiffness induces ROCK activity, which stabilizes SNAIL1 protein indirectly by increasing intracellular tension, integrin clustering and integrin signaling to ERK2 (also known as MAPK1). Increased ERK2 activity leads to nuclear accumulation of SNAIL1, and, thus, avoidance of cytosolic proteasome degradation. SNAIL1 also influences the level and activity of YAP1 in CAFs exposed to a stiff matrix. This work describes a mechanism whereby increased tumor fibrosis can perpetuate activation of CAFs to sustain tumor fibrosis and promote tumor metastasis through regulation of SNAIL1 protein level and activity. Twit Text FOAVip Mechanical signals regulate and activate SNAIL1 protein to control the fibrogenic response of cancer-associated fibroblasts ????J Cell Sci http://www.kidney.de/pget.php?&tw=1&pmid=27076520 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27076520 #FOAvip English Wikipedia <ref>{{Cite pmid|27076520 }}</ref> Mechanical signals regulate and activate SNAIL1 protein to control the fibrogenic response of cancer-associated fibroblasts #MMPMID27076520 Zhang K ; Grither WR ; Van Hove S ; Biswas H ; Ponik SM ; Eliceiri KW ; Keely PJ ; Longmore GD J Cell Sci 2016[May]; 129 (10 ): 1989-2002 PMID27076520 show ga Increased deposition of collagen in extracellular matrix (ECM) leads to increased tissue stiffness and occurs in breast tumors. When present, this increases tumor invasion and metastasis. Precisely how this deposition is regulated and maintained in tumors is unclear. Much has been learnt about mechanical signal transduction in cells, but transcriptional responses and the pathophysiological consequences are just becoming appreciated. Here, we show that the SNAIL1 (also known as SNAI1) protein level increases and accumulates in nuclei of breast tumor cells and cancer-associated fibroblasts (CAFs) following exposure to stiff ECM in culture and in vivo SNAIL1 is required for the fibrogenic response of CAFs when exposed to a stiff matrix. ECM stiffness induces ROCK activity, which stabilizes SNAIL1 protein indirectly by increasing intracellular tension, integrin clustering and integrin signaling to ERK2 (also known as MAPK1). Increased ERK2 activity leads to nuclear accumulation of SNAIL1, and, thus, avoidance of cytosolic proteasome degradation. SNAIL1 also influences the level and activity of YAP1 in CAFs exposed to a stiff matrix. This work describes a mechanism whereby increased tumor fibrosis can perpetuate activation of CAFs to sustain tumor fibrosis and promote tumor metastasis through regulation of SNAIL1 protein level and activity. |Adaptor Proteins, Signal Transducing/*genetics [MESH] |Breast Neoplasms/*genetics/pathology [MESH] |Cancer-Associated Fibroblasts/metabolism/pathology [MESH] |Cell Line, Tumor [MESH] |Collagen/metabolism [MESH] |Extracellular Matrix/genetics/metabolism [MESH] |Humans [MESH] |Mitogen-Activated Protein Kinase 1/*genetics [MESH] |Phosphoproteins/*genetics [MESH] |Signal Transduction [MESH] |Snail Family Transcription Factors/*genetics [MESH] |Transcription Factors [MESH] |YAP-Signaling Proteins [MESH]Mechanical signals regulate and activate SNAIL1 protein to control the(epmc).pdf DeepDyve Pubget Overpricing