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10.1038/s41419-017-0068-6 http://scihub22266oqcxt.onion/10.1038/s41419-017-0068-6 C5833725!5833725 !29339720     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29339720 &cmd=llinks): Failed to open stream: HTTP request failed! 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Plumbagin inhibits the proliferation and survival of esophageal cancer cells by blocking STAT3-PLK1-AKT signaling |pdf=|usr=}}{{29339720 }} gab.com Text Plumbagin inhibits the proliferation and survival of esophageal cancer cells by blocking STAT3-PLK1-AKT signaling JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29339720 #FOAvip Esophageal squamous cell carcinoma (ESCC) is one of the deadliest cancers, and it requires novel treatment approaches and effective drugs. In the present study, we found that treatment with plumbagin, a natural compound, reduced proliferation and survival of the KYSE150 and KYSE450 ESCC cell lines in a dose-dependent manner in vitro. The drug also effectively inhibited the viability of primary ESCC cells from fresh biopsy specimens. Furthermore, plumbagin-induced mitotic arrest and massive apoptosis in ESCC cells. Notably, the drug significantly suppressed the colony formation capacity of ESCC cells in vitro and the growth of KYSE150 xenograft tumors in vivo. At the molecular level, we found that exposure to plumbagin decreased both polo-like kinase 1 (PLK1) and phosphorylated protein kinase B (p-AKT) expression in both ESCC cell lines. Enforced PLK1 expression in ESCC cells not only markedly rescued cells from plumbagin-induced apoptosis and proliferation inhibition but also restored the impaired AKT activity. Furthermore, signal transducer and activator of transcription 3 (STAT3), a transcription factor of PLK1, was also inactivated in plumbagin-treated ESCC cells; however, the overexpression of a constitutively activated STAT3 mutant, STAT3C, reinstated the plumbagin-elicited blockade of PLK1-AKT signaling in ESCC cells. Taken together, these findings indicate that plumbagin inhibits proliferation and potentiates apoptosis in human ESCC cells in vitro and in vivo. Plumbagin may exert these antitumor effects by abrogating STAT3-PLK1-AKT signaling, which suggests that plumbagin may be a novel, promising anticancer agent for the treatment of ESCC. Twit Text FOAVip Plumbagin inhibits the proliferation and survival of esophageal cancer cells by blocking STAT3-PLK1-AKT signaling ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29339720 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29339720 #FOAvip English Wikipedia <ref>{{Cite pmid|29339720 }}</ref> Plumbagin inhibits the proliferation and survival of esophageal cancer cells by blocking STAT3-PLK1-AKT signaling #MMPMID29339720 Cao YY ; Yu J ; Liu TT ; Yang KX ; Yang LY ; Chen Q ; Shi F ; Hao JJ ; Cai Y ; Wang MR ; Lu WH ; Zhang Y Cell Death Dis 2018[Jan]; 9 (2 ): 17 PMID29339720 show ga Esophageal squamous cell carcinoma (ESCC) is one of the deadliest cancers, and it requires novel treatment approaches and effective drugs. In the present study, we found that treatment with plumbagin, a natural compound, reduced proliferation and survival of the KYSE150 and KYSE450 ESCC cell lines in a dose-dependent manner in vitro. The drug also effectively inhibited the viability of primary ESCC cells from fresh biopsy specimens. Furthermore, plumbagin-induced mitotic arrest and massive apoptosis in ESCC cells. Notably, the drug significantly suppressed the colony formation capacity of ESCC cells in vitro and the growth of KYSE150 xenograft tumors in vivo. At the molecular level, we found that exposure to plumbagin decreased both polo-like kinase 1 (PLK1) and phosphorylated protein kinase B (p-AKT) expression in both ESCC cell lines. Enforced PLK1 expression in ESCC cells not only markedly rescued cells from plumbagin-induced apoptosis and proliferation inhibition but also restored the impaired AKT activity. Furthermore, signal transducer and activator of transcription 3 (STAT3), a transcription factor of PLK1, was also inactivated in plumbagin-treated ESCC cells; however, the overexpression of a constitutively activated STAT3 mutant, STAT3C, reinstated the plumbagin-elicited blockade of PLK1-AKT signaling in ESCC cells. Taken together, these findings indicate that plumbagin inhibits proliferation and potentiates apoptosis in human ESCC cells in vitro and in vivo. Plumbagin may exert these antitumor effects by abrogating STAT3-PLK1-AKT signaling, which suggests that plumbagin may be a novel, promising anticancer agent for the treatment of ESCC. |Animals [MESH] |Apoptosis/drug effects [MESH] |Carcinogenesis/drug effects/metabolism/pathology [MESH] |Cell Cycle Checkpoints/drug effects [MESH] |Cell Cycle Proteins/*metabolism [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation/drug effects [MESH] |Cell Survival/drug effects [MESH] |Down-Regulation/drug effects [MESH] |Esophageal Neoplasms/*metabolism/*pathology [MESH] |Esophageal Squamous Cell Carcinoma/pathology [MESH] |Female [MESH] |Humans [MESH] |Mice, Nude [MESH] |Naphthoquinones/*pharmacology [MESH] |Polo-Like Kinase 1 [MESH] |Protein Serine-Threonine Kinases/*metabolism [MESH] |Proto-Oncogene Proteins c-akt/*metabolism [MESH] |Proto-Oncogene Proteins/*metabolism [MESH] |STAT3 Transcription Factor/*metabolism [MESH] |Signal Transduction/*drug effects [MESH]Plumbagin inhibits the proliferation and survival of esophageal cancer(epmc).pdf DeepDyve Pubget Overpricing