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10.1038/aps.2016.122 http://scihub22266oqcxt.onion/10.1038/aps.2016.122 C5309754!5309754 !27890917     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27890917 &cmd=llinks): Failed to open stream: HTTP request failed! 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Sulforaphane suppresses EMT and metastasis in human lung cancer through miR-616-5p-mediated GSK3?/?-catenin signaling pathways |pdf=|usr=}}{{27890917 }} gab.com Text Sulforaphane suppresses EMT and metastasis in human lung cancer through miR-616-5p-mediated GSK3 / -catenin signaling pathways JO: Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=27890917 #FOAvip Sulforaphane is a common antioxidant selectively abundant in cruciferous plants, which exhibits effective anti-cancer actions in control of tumorigenesis or progression of various cancers. A recent study has shown that sulforaphane attenuates the EGFR signaling pathway in non-small cell lung cancer (NSCLC), suggesting its potential anti-metastatic effects. In this study we assessed the involvement of sulforaphane and miR-616-5p in epithelial-mesenchymal transition (EMT) and NSCLC metastasis. Sulforaphane suppressed the cell proliferation in human NSCLC cell lines H1299, 95C and 95D with IC(50) values of 9.52±1.23, 9.04±1.90 and 17.35±2.03 ?mol/L, respectively. At low concentrations (1-5 ?mol/L), sulforaphane dose-dependently inhibited the migration and invasion of 95D and H1299 cells with relatively high metastatic potential. The anti-metastatic action of sulforaphane was confirmed in 95D and H1299 cell xenografts in vivo. In fresh NSCLC tissue samples from 179 patients, miR-616-5p levels were upregulated in late-stage NSCLCs, and strongly correlated with risk of NSCLC recurrence and metastasis. Consistent with the clinic observation, miR-616-5p levels in the 3 NSCLC cell lines were correlated with their metastatic ability, and were decreased by sulforaphane treatment. Silencing miR-616-5p markedly suppressed the migration and invasion of 95D cells in vitro and NSCLC metastasis in vivo. Further studies revealed that miR-616-5p directly targeted GSK3? and decreased its expression, whereas sulforaphane decreased miR-616-5p levels by histone modification, and followed by inactivation of the GSK3?/?-catenin signaling pathway and inhibition of EMT, which was characterized by loss of epithelial markers and acquisition of a mesenchymal phenotype in NSCLC cells. Our findings suggest that sulforaphane is a potential adjuvant chemotherapeutic agent for the prevention of NSCLC recurrence and metastasis, and miR-616-5p can be clinically utilized as a biomarker or therapeutic target to inhibit metastasis. Twit Text FOAVip Sulforaphane suppresses EMT and metastasis in human lung cancer through miR-616-5p-mediated GSK3 / -catenin signaling pathways ????Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=27890917 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27890917 #FOAvip English Wikipedia <ref>{{Cite pmid|27890917 }}</ref> Sulforaphane suppresses EMT and metastasis in human lung cancer through miR-616-5p-mediated GSK3?/?-catenin signaling pathways #MMPMID27890917 Wang DX ; Zou YJ ; Zhuang XB ; Chen SX ; Lin Y ; Li WL ; Lin JJ ; Lin ZQ Acta Pharmacol Sin 2017[Feb]; 38 (2 ): 241-251 PMID27890917 show ga Sulforaphane is a common antioxidant selectively abundant in cruciferous plants, which exhibits effective anti-cancer actions in control of tumorigenesis or progression of various cancers. A recent study has shown that sulforaphane attenuates the EGFR signaling pathway in non-small cell lung cancer (NSCLC), suggesting its potential anti-metastatic effects. In this study we assessed the involvement of sulforaphane and miR-616-5p in epithelial-mesenchymal transition (EMT) and NSCLC metastasis. Sulforaphane suppressed the cell proliferation in human NSCLC cell lines H1299, 95C and 95D with IC(50) values of 9.52±1.23, 9.04±1.90 and 17.35±2.03 ?mol/L, respectively. At low concentrations (1-5 ?mol/L), sulforaphane dose-dependently inhibited the migration and invasion of 95D and H1299 cells with relatively high metastatic potential. The anti-metastatic action of sulforaphane was confirmed in 95D and H1299 cell xenografts in vivo. In fresh NSCLC tissue samples from 179 patients, miR-616-5p levels were upregulated in late-stage NSCLCs, and strongly correlated with risk of NSCLC recurrence and metastasis. Consistent with the clinic observation, miR-616-5p levels in the 3 NSCLC cell lines were correlated with their metastatic ability, and were decreased by sulforaphane treatment. Silencing miR-616-5p markedly suppressed the migration and invasion of 95D cells in vitro and NSCLC metastasis in vivo. Further studies revealed that miR-616-5p directly targeted GSK3? and decreased its expression, whereas sulforaphane decreased miR-616-5p levels by histone modification, and followed by inactivation of the GSK3?/?-catenin signaling pathway and inhibition of EMT, which was characterized by loss of epithelial markers and acquisition of a mesenchymal phenotype in NSCLC cells. Our findings suggest that sulforaphane is a potential adjuvant chemotherapeutic agent for the prevention of NSCLC recurrence and metastasis, and miR-616-5p can be clinically utilized as a biomarker or therapeutic target to inhibit metastasis. |Animals [MESH] |Carcinoma, Non-Small-Cell Lung/drug therapy/metabolism/pathology [MESH] |Cell Line, Tumor [MESH] |Cell Survival/drug effects [MESH] |Epithelial-Mesenchymal Transition/*drug effects [MESH] |Gene Expression Regulation, Neoplastic/drug effects [MESH] |Glycogen Synthase Kinase 3 beta/*metabolism [MESH] |Humans [MESH] |Isothiocyanates/pharmacology/*therapeutic use [MESH] |Lung Neoplasms/*drug therapy/metabolism/pathology [MESH] |Mice [MESH] |MicroRNAs/*metabolism [MESH] |Neoplasm Metastasis/*drug therapy [MESH] |Neoplasm Recurrence, Local/drug therapy [MESH] |Signal Transduction/*drug effects [MESH] |Sulfoxides [MESH] |Xenograft Model Antitumor Assays [MESH]Sulforaphane suppresses EMT and metastasis in human lung cancer throug(epmc).pdf DeepDyve Pubget Overpricing