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10.2147/OTT.S137146 http://scihub22266oqcxt.onion/10.2147/OTT.S137146 C5841350!5841350 !29535539     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29535539 &cmd=llinks): Failed to open stream: HTTP request failed! 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SIRT1 overexpression protects non-small cell lung cancer cells against osteopontin-induced epithelial-mesenchymal transition by suppressing NF-?B signaling |pdf=|usr=}}{{29535539 }} gab.com Text SIRT1 overexpression protects non-small cell lung cancer cells against osteopontin-induced epithelial-mesenchymal transition by suppressing NF- B signaling JO: Onco Targets Ther http://www.kidney.de/pget.php?&tw=1&pmid=29535539 #FOAvip Osteopontin (OPN) is a promoter for tumor progression. It has been reported to promote non-small cell lung cancer (NSCLC) progression via the activation of nuclear factor-?B (NF-?B) signaling. As the increased acetylation of NF-?B p65 is linked to NF-?B activation, the regulation of NF-?B p65 acetylation could be a potential treatment target for OPN-induced NSCLC progression. Sirtuin 1 (SIRT1) is a deacetylase, and the role of SIRT1 in tumor progression is still controversial. The effect and mechanism of SIRT1 on OPN-induced tumor progression remains unknown. The results presented in this research demonstrated that OPN inhibited SIRT1 expression and promoted NF-?B p65 acetylation in NSCLC cell lines (A549 and NCI-H358). In this article, overexpression of SIRT1 was induced by infection of SIRT1-overexpressing lentiviral vectors. The overexpression of SIRT1 protected NSCLC cells against OPN-induced NF-?B p65 acetylation and epithelial-mesenchymal transition (EMT), as indicated by the reduction of OPN-induced changes in the expression levels of EMT-related markers and cellular morphology. Furthermore, SIRT1 overexpression significantly attenuated OPN-induced cell proliferation, migration and invasion. Moreover, overexpression of SIRT1 inhibited OPN-induced NF-?B activation. As OPN induced NSCLC cell EMT through activation of NF-?B signaling, OPN-induced SIRT1 downregulation may play an important role in NSCLC cell EMT via NF-?B signaling. The results suggest that SIRT1 could be a tumor suppressor to attenuate OPN-induced NSCLC progression through the regulation of NF-?B signaling. Twit Text FOAVip SIRT1 overexpression protects non-small cell lung cancer cells against osteopontin-induced epithelial-mesenchymal transition by suppressing NF- B signaling ????Onco Targets Ther http://www.kidney.de/pget.php?&tw=1&pmid=29535539 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29535539 #FOAvip English Wikipedia <ref>{{Cite pmid|29535539 }}</ref> SIRT1 overexpression protects non-small cell lung cancer cells against osteopontin-induced epithelial-mesenchymal transition by suppressing NF-?B signaling #MMPMID29535539 Li X ; Jiang Z ; Li X ; Zhang X Onco Targets Ther 2018[]; 11 (ä): 1157-1171 PMID29535539 show ga Osteopontin (OPN) is a promoter for tumor progression. It has been reported to promote non-small cell lung cancer (NSCLC) progression via the activation of nuclear factor-?B (NF-?B) signaling. As the increased acetylation of NF-?B p65 is linked to NF-?B activation, the regulation of NF-?B p65 acetylation could be a potential treatment target for OPN-induced NSCLC progression. Sirtuin 1 (SIRT1) is a deacetylase, and the role of SIRT1 in tumor progression is still controversial. The effect and mechanism of SIRT1 on OPN-induced tumor progression remains unknown. The results presented in this research demonstrated that OPN inhibited SIRT1 expression and promoted NF-?B p65 acetylation in NSCLC cell lines (A549 and NCI-H358). In this article, overexpression of SIRT1 was induced by infection of SIRT1-overexpressing lentiviral vectors. The overexpression of SIRT1 protected NSCLC cells against OPN-induced NF-?B p65 acetylation and epithelial-mesenchymal transition (EMT), as indicated by the reduction of OPN-induced changes in the expression levels of EMT-related markers and cellular morphology. Furthermore, SIRT1 overexpression significantly attenuated OPN-induced cell proliferation, migration and invasion. Moreover, overexpression of SIRT1 inhibited OPN-induced NF-?B activation. As OPN induced NSCLC cell EMT through activation of NF-?B signaling, OPN-induced SIRT1 downregulation may play an important role in NSCLC cell EMT via NF-?B signaling. The results suggest that SIRT1 could be a tumor suppressor to attenuate OPN-induced NSCLC progression through the regulation of NF-?B signaling. äSIRT1 overexpression protects non-small cell lung cancer cells against(epmc).pdf DeepDyve Pubget Overpricing