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10.2741/4641 http://scihub22266oqcxt.onion/10.2741/4641 C5632947!5632947 !28930597     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28930597 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Front+Biosci+(Landmark+Ed) 2018 ; 23 (7 ): 1241-1256 Nephropedia Template TP {{tp|p=28930597 |t=2018. The store-operated calcium channels in cancer metastasis: from cell migration, invasion to metastatic colonization |pdf=|usr=}}{{28930597 }} gab.com Text The store-operated calcium channels in cancer metastasis: from cell migration, invasion to metastatic colonization JO: Front Biosci (Landmark Ed) http://www.kidney.de/pget.php?&tw=1&pmid=28930597 #FOAvip Store-operated calcium entry (SOCE) is the predominant calcium entry mechanism in most cancer cells. SOCE is mediated by the endoplasmic reticulum calcium sensor STIMs (STIM1 and 2) and plasma membrane channel forming unit Orais (Orai 1-3). In recent years there is increasing evidence indicating that SOCE in cancer cells is dysregulated to promote cancer cell migration, invasion and metastasis. The overexpression of STIM and Orai proteins has been reported to correlate with the metastatic progression of various cancers. The hyperactive SOCE may promote metastatic dissemination and colonization by reorganizing the actin cytoskeleton, degrading the extracellular matrix and remodeling the tumor microenvironment. Here we discuss how these recent progresses provide novel insights to our understanding of tumor metastasis. Twit Text FOAVip The store-operated calcium channels in cancer metastasis: from cell migration, invasion to metastatic colonization ????Front Biosci (Landmark Ed) http://www.kidney.de/pget.php?&tw=1&pmid=28930597 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28930597 #FOAvip English Wikipedia <ref>{{Cite pmid|28930597 }}</ref> The store-operated calcium channels in cancer metastasis: from cell migration, invasion to metastatic colonization #MMPMID28930597 Mo P ; Yang S Front Biosci (Landmark Ed) 2018[Jan]; 23 (7 ): 1241-1256 PMID28930597 show ga Store-operated calcium entry (SOCE) is the predominant calcium entry mechanism in most cancer cells. SOCE is mediated by the endoplasmic reticulum calcium sensor STIMs (STIM1 and 2) and plasma membrane channel forming unit Orais (Orai 1-3). In recent years there is increasing evidence indicating that SOCE in cancer cells is dysregulated to promote cancer cell migration, invasion and metastasis. The overexpression of STIM and Orai proteins has been reported to correlate with the metastatic progression of various cancers. The hyperactive SOCE may promote metastatic dissemination and colonization by reorganizing the actin cytoskeleton, degrading the extracellular matrix and remodeling the tumor microenvironment. Here we discuss how these recent progresses provide novel insights to our understanding of tumor metastasis. |Animals [MESH] |Calcium Channels/*metabolism [MESH] |Calcium/*metabolism [MESH] |Cell Movement [MESH] |Endoplasmic Reticulum/*metabolism [MESH] |Epithelial-Mesenchymal Transition [MESH] |Focal Adhesions [MESH] |Humans [MESH] |Models, Biological [MESH] |Neoplasm Invasiveness [MESH] |Neoplasm Metastasis [MESH] |Neoplasms/*metabolism/pathology [MESH] |ORAI1 Protein/metabolism [MESH]The store-operated calcium channels in cancer metastasis: from cell mi(epmc).pdf DeepDyve Pubget Overpricing