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10.18632/oncotarget.12895 http://scihub22266oqcxt.onion/10.18632/oncotarget.12895 C5348340!5348340 !27793015     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27793015 &cmd=llinks): Failed to open stream: HTTP request failed! 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TRPC1-STIM1 activation modulates transforming growth factor ?-induced epithelial-to-mesenchymal transition |pdf=|usr=}}{{27793015 }} gab.com Text TRPC1-STIM1 activation modulates transforming growth factor -induced epithelial-to-mesenchymal transition JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27793015 #FOAvip Activation of Epithelial-to-Mesenchymal Transition (EMT) is important for tumor metastasis. Although growth factors such as TGF? and EGF have been shown to induce EMT in breast epithelial cells, the mechanism resulting in migration is not well understood. Herein, we provide evidence that Ca2+ entry into the cell, especially upon store-depletion, plays an important role in TGF?-induced EMT by promoting cellular migration and potentially leading to metastasis. The increased migration by TGF? in non-cancerous cells was due to the loss of E-cadherin along with a subsequent increase in N-cadherin levels. Importantly, TGF?-treatment increases store-mediated Ca2+ entry, which was essential for the activation of calpain leading to the loss of E-cadherin and MMP activation. Inhibition of Ca2+ entry by using Ca2+ channel blocker SKF-96365, significantly decreased Ca2+ entry, decreased TGF?-induced calpain activation, and suppressed the loss of E-cadherin along with inhibiting cell migration. Furthermore, TRPC1 function as an endogenous Ca2+ entry channel and silencing of either TRPC1 or its activator, STIM1, significantly decreased TGF? induced Ca2+ entry, inhibited TGF?-mediated calpain activation and cell migration. In contrast, overexpression of TRPC1 showed increased Ca2+ entry and promoted TGF?-mediated cell migration. Moreover, increased TRPC1 expression was observed in ductal carcinoma cells. Together these results suggest that disrupting Ca2+ influx via TRPC1/STIM1 mechanism reduces calpain activity, which could restore intercellular junction proteins thereby inhibiting EMT induced motility. Twit Text FOAVip TRPC1-STIM1 activation modulates transforming growth factor -induced epithelial-to-mesenchymal transition ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27793015 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27793015 #FOAvip English Wikipedia <ref>{{Cite pmid|27793015 }}</ref> TRPC1-STIM1 activation modulates transforming growth factor ?-induced epithelial-to-mesenchymal transition #MMPMID27793015 Schaar A ; Sukumaran P ; Sun Y ; Dhasarathy A ; Singh BB Oncotarget 2016[Dec]; 7 (49 ): 80554-80567 PMID27793015 show ga Activation of Epithelial-to-Mesenchymal Transition (EMT) is important for tumor metastasis. Although growth factors such as TGF? and EGF have been shown to induce EMT in breast epithelial cells, the mechanism resulting in migration is not well understood. Herein, we provide evidence that Ca2+ entry into the cell, especially upon store-depletion, plays an important role in TGF?-induced EMT by promoting cellular migration and potentially leading to metastasis. The increased migration by TGF? in non-cancerous cells was due to the loss of E-cadherin along with a subsequent increase in N-cadherin levels. Importantly, TGF?-treatment increases store-mediated Ca2+ entry, which was essential for the activation of calpain leading to the loss of E-cadherin and MMP activation. Inhibition of Ca2+ entry by using Ca2+ channel blocker SKF-96365, significantly decreased Ca2+ entry, decreased TGF?-induced calpain activation, and suppressed the loss of E-cadherin along with inhibiting cell migration. Furthermore, TRPC1 function as an endogenous Ca2+ entry channel and silencing of either TRPC1 or its activator, STIM1, significantly decreased TGF? induced Ca2+ entry, inhibited TGF?-mediated calpain activation and cell migration. In contrast, overexpression of TRPC1 showed increased Ca2+ entry and promoted TGF?-mediated cell migration. Moreover, increased TRPC1 expression was observed in ductal carcinoma cells. Together these results suggest that disrupting Ca2+ influx via TRPC1/STIM1 mechanism reduces calpain activity, which could restore intercellular junction proteins thereby inhibiting EMT induced motility. |Antigens, CD/metabolism [MESH] |Breast Neoplasms/genetics/*metabolism/pathology [MESH] |Cadherins/metabolism [MESH] |Calcium Signaling/drug effects [MESH] |Calpain/metabolism [MESH] |Cell Line, Tumor [MESH] |Cell Movement/drug effects [MESH] |Epithelial-Mesenchymal Transition/*drug effects [MESH] |Female [MESH] |Humans [MESH] |Matrix Metalloproteinases/metabolism [MESH] |Membrane Potentials [MESH] |Neoplasm Metastasis [MESH] |Neoplasm Proteins/genetics/*metabolism [MESH] |RNA Interference [MESH] |Stromal Interaction Molecule 1/genetics/*metabolism [MESH] |TRPC Cation Channels/genetics/*metabolism [MESH] |Time Factors [MESH] |Transfection [MESH]TRPC1-STIM1 activation modulates transforming growth factor ?-induced (epmc).pdf DeepDyve Pubget Overpricing