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10.3892/ol.2018.8885 http://scihub22266oqcxt.onion/10.3892/ol.2018.8885 C6036567!6036567 !30013652     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30013652 &cmd=llinks): Failed to open stream: HTTP request failed! 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Juglone suppresses epithelial-mesenchymal transition in prostate cancer cells via the protein kinase B/glycogen synthase kinase-3?/Snail signaling pathway |pdf=|usr=}}{{30013652 }} gab.com Text Juglone suppresses epithelial-mesenchymal transition in prostate cancer cells via the protein kinase B/glycogen synthase kinase-3 /Snail signaling pathway JO: Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=30013652 #FOAvip Epithelial-mesenchymal transition (EMT) serves an important role in the metastasis of prostate cancer. Juglone is a natural compound isolated from plants that is reported to possess potent cytotoxic properties. However, there are no studies on the anti-EMT effect of juglone in prostate cancer, or its potential underlying mechanisms of action. In the present study, the effect of juglone on the EMT of prostate cancer cells was investigated. Transwell assays were used to demonstrate that juglone inhibits the migration and invasion of the prostate cancer (PC) LNCaP and LNCaP-AI cell lines. Results from western blot analysis demonstrated that juglone increases the expression of the epithelial marker E-cadherin while decreasing the expression of mesenchymal markers (N-cadherin and Vimentin) in a dose-dependent manner. The data from the present study also revealed that juglone downregulates the expression of Snail, a repressor of E-cadherin and an inducer of EMT. Furthermore, juglone prevented inactivation of glycogen synthase kinase-3? (GSK-3?), an endogenous inhibitor of Snail in a dose-dependent manner. Lithium chloride (LiCl), a GSK-3? inhibitor, prevented juglone-mediated downregulation of Snail expression and upregulation of E-cadherin. In addition, phosphorylation and subsequent activation of protein kinase B (Akt), which is known to phosphorylate GSK-3? at serine 9 (Ser9), leading to its inhibition, were significantly decreased by juglone in LNCaP and LNCaP-AI cells. Inhibition of the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt pathway by LY294002 augmented juglone-mediated GSK-3? activity by inhibiting Ser9 phosphorylation. These findings indicated that juglone suppresses EMT via the Akt/GSK-3?/Snail pathway, consequently decreasing the invasiveness of PC cells. Twit Text FOAVip Juglone suppresses epithelial-mesenchymal transition in prostate cancer cells via the protein kinase B/glycogen synthase kinase-3 /Snail signaling pathway ????Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=30013652 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30013652 #FOAvip English Wikipedia <ref>{{Cite pmid|30013652 }}</ref> Juglone suppresses epithelial-mesenchymal transition in prostate cancer cells via the protein kinase B/glycogen synthase kinase-3?/Snail signaling pathway #MMPMID30013652 Fang F ; Chen S ; Ma J ; Cui J ; Li Q ; Meng G ; Wang L Oncol Lett 2018[Aug]; 16 (2 ): 2579-2584 PMID30013652 show ga Epithelial-mesenchymal transition (EMT) serves an important role in the metastasis of prostate cancer. Juglone is a natural compound isolated from plants that is reported to possess potent cytotoxic properties. However, there are no studies on the anti-EMT effect of juglone in prostate cancer, or its potential underlying mechanisms of action. In the present study, the effect of juglone on the EMT of prostate cancer cells was investigated. Transwell assays were used to demonstrate that juglone inhibits the migration and invasion of the prostate cancer (PC) LNCaP and LNCaP-AI cell lines. Results from western blot analysis demonstrated that juglone increases the expression of the epithelial marker E-cadherin while decreasing the expression of mesenchymal markers (N-cadherin and Vimentin) in a dose-dependent manner. The data from the present study also revealed that juglone downregulates the expression of Snail, a repressor of E-cadherin and an inducer of EMT. Furthermore, juglone prevented inactivation of glycogen synthase kinase-3? (GSK-3?), an endogenous inhibitor of Snail in a dose-dependent manner. Lithium chloride (LiCl), a GSK-3? inhibitor, prevented juglone-mediated downregulation of Snail expression and upregulation of E-cadherin. In addition, phosphorylation and subsequent activation of protein kinase B (Akt), which is known to phosphorylate GSK-3? at serine 9 (Ser9), leading to its inhibition, were significantly decreased by juglone in LNCaP and LNCaP-AI cells. Inhibition of the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt pathway by LY294002 augmented juglone-mediated GSK-3? activity by inhibiting Ser9 phosphorylation. These findings indicated that juglone suppresses EMT via the Akt/GSK-3?/Snail pathway, consequently decreasing the invasiveness of PC cells. äJuglone suppresses epithelial-mesenchymal transition in prostate cance(epmc).pdf DeepDyve Pubget Overpricing