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10.1038/s41598-018-25373-0 http://scihub22266oqcxt.onion/10.1038/s41598-018-25373-0 29743493!5943603!29743493     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29743493&cmd=llinks): Failed to open stream: HTTP request failed! 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The Kindlin-2 regulation of epithelial-to-mesenchymal transition in breast cancer metastasis is mediated through miR-200b |pdf=|usr=}}{{29743493}} gab.com Text The Kindlin-2 regulation of epithelial-to-mesenchymal transition in breast cancer metastasis is mediated through miR-200b JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29743493 #FOAvip Metastasis is the main cause of death in cancer patients, including breast cancer (BC). Despite recent progress in understanding the biological and molecular determinants of BC metastasis, effective therapeutic treatments are yet to be developed. Among the multitude of molecular mechanisms that regulate cancer metastasis, the epithelial-to-mesenchymal transition (EMT) program plays a key role in the activation of the biological steps leading to the metastatic phenotype. Kindlin-2 has been associated with the pathogenesis of several types of cancers, including BC. The role of Kindlin-2 in the regulation of BC metastasis, and to a lesser extent in EMT is not well understood. In this study, we show that Kindlin-2 is closely associated with the development of the metastatic phenotype in BC. We report that knockout of Kindlin-2 in either human or mouse BC cells, significantly inhibits metastasis in both human and mouse models of BC metastasis. We also report that the Kindlin-2-mediated inhibition of metastasis is the result of inhibition of expression of key molecular markers of the EMT program. Mechanistically, we show that miR-200b, a master regulator of EMT, directly targets and inhibits the expression of Kindlin-2, leading to the subsequent inhibition of EMT and metastasis. Together, our data support the targeting of Kindlin-2 as a therapeutic strategy against BC metastasis. Twit Text FOAVip The Kindlin-2 regulation of epithelial-to-mesenchymal transition in breast cancer metastasis is mediated through miR-200b ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29743493 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29743493 #FOAvip English Wikipedia <ref>{{Cite pmid|29743493}}</ref> The Kindlin-2 regulation of epithelial-to-mesenchymal transition in breast cancer metastasis is mediated through miR-200b #MMPMID29743493 Sossey-Alaoui K; Pluskota E; Szpak D; Schiemann WP; Plow EF Sci Rep 2018[May]; 8 (1): 7360 PMID29743493show ga Metastasis is the main cause of death in cancer patients, including breast cancer (BC). Despite recent progress in understanding the biological and molecular determinants of BC metastasis, effective therapeutic treatments are yet to be developed. Among the multitude of molecular mechanisms that regulate cancer metastasis, the epithelial-to-mesenchymal transition (EMT) program plays a key role in the activation of the biological steps leading to the metastatic phenotype. Kindlin-2 has been associated with the pathogenesis of several types of cancers, including BC. The role of Kindlin-2 in the regulation of BC metastasis, and to a lesser extent in EMT is not well understood. In this study, we show that Kindlin-2 is closely associated with the development of the metastatic phenotype in BC. We report that knockout of Kindlin-2 in either human or mouse BC cells, significantly inhibits metastasis in both human and mouse models of BC metastasis. We also report that the Kindlin-2-mediated inhibition of metastasis is the result of inhibition of expression of key molecular markers of the EMT program. Mechanistically, we show that miR-200b, a master regulator of EMT, directly targets and inhibits the expression of Kindlin-2, leading to the subsequent inhibition of EMT and metastasis. Together, our data support the targeting of Kindlin-2 as a therapeutic strategy against BC metastasis. |Animals[MESH] |Breast Neoplasms/*genetics/*pathology[MESH] |Cell Adhesion[MESH] |Cell Line, Tumor[MESH] |Cytoskeletal Proteins/*genetics[MESH] |Disease Progression[MESH] |Down-Regulation/genetics[MESH] |Epithelial-Mesenchymal Transition/*genetics[MESH] |Extracellular Matrix/metabolism[MESH] |Female[MESH] |Focal Adhesions/metabolism[MESH] |Mice[MESH] |MicroRNAs/*genetics[MESH] |Muscle Proteins/*genetics[MESH] |Neoplasm Metastasis[MESH]The Kindlin-2 regulation of epithelial-to-mesenchymal transition in br(epmc).pdf DeepDyve Pubget Overpricing