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10.1158/1535-7163.MCT-14-0496 http://scihub22266oqcxt.onion/10.1158/1535-7163.MCT-14-0496 C4557740!4557740!25376608     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25376608&cmd=llinks): Failed to open stream: HTTP request failed! 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The Protein Phosphatase 2A Inhibitor LB100 Sensitizes Ovarian Carcinoma Cells to Cisplatin-Mediated Cytotoxicity |pdf=|usr=}}{{25376608}} gab.com Text The Protein Phosphatase 2A Inhibitor LB100 Sensitizes Ovarian Carcinoma Cells to Cisplatin-Mediated Cytotoxicity JO: Mol Cancer Ther http://www.kidney.de/pget.php?&tw=1&pmid=25376608 #FOAvip Despite early positive response to platinum-based chemotherapy, the majority of ovarian carcinomas develop resistance and progress to fatal disease. Protein phosphatase 2A (PP2A) is a ubiquitous phosphatase involved in the regulation of DNA damage response and cell cycle checkpoint pathways. Recent studies have shown that LB100, a small molecule inhibitor of PP2A, sensitizes cancer cells to radiation-mediated DNA damage. We hypothesized that LB100 could sensitize ovarian cancer cells to cisplatin treatment. We performed in vitro studies in SKOV-3, OVCAR-8, and PEO1, 4, and 6 ovarian cancer lines to assess cytotoxicity potentiation, cell-death mechanism(s), cell cycle regulation, and DNA damage response signaling. In vivo studies were conducted in an intraperitoneal metastatic mouse model using SKOV-3/f-Luc cells. LB100 sensitized ovarian carcinoma lines to cisplatin-mediated cell death. Sensitization via LB100 was mediated by abrogation of cell cycle arrest induced by cisplatin. Loss of the cisplatin-induced checkpoint correlated with decreased Wee1 expression, increased cdc2 activation, and increased mitotic entry (p-histone H3). LB100 also induced constitutive hyperphosphorylation of DNA damage response proteins (BRCA1, Chk2, ?H2AX), altered the chronology and persistence of JNK activation, and modulated the expression of 14-3-3 binding sites. In vivo, cisplatin sensitization via LB100 significantly enhanced tumor growth inhibition and prevented disease progression after treatment cessation. Our results suggest that LB100 sensitizes ovarian cancer cells to cisplatin in vitro and in vivo by modulation of the DNA damage response pathway and cell cycle checkpoint abrogation. Twit Text FOAVip The Protein Phosphatase 2A Inhibitor LB100 Sensitizes Ovarian Carcinoma Cells to Cisplatin-Mediated Cytotoxicity ????Mol Cancer Ther http://www.kidney.de/pget.php?&tw=1&pmid=25376608 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25376608 #FOAvip English Wikipedia <ref>{{Cite pmid|25376608}}</ref> The Protein Phosphatase 2A Inhibitor LB100 Sensitizes Ovarian Carcinoma Cells to Cisplatin-Mediated Cytotoxicity #MMPMID25376608 Chang KE; Wei BR; Madigan JP; Hall MD; Simpson RM; Zhuang Z; Gottesman MM Mol Cancer Ther 2015[Jan]; 14 (1): 90-100 PMID25376608show ga Despite early positive response to platinum-based chemotherapy, the majority of ovarian carcinomas develop resistance and progress to fatal disease. Protein phosphatase 2A (PP2A) is a ubiquitous phosphatase involved in the regulation of DNA damage response and cell cycle checkpoint pathways. Recent studies have shown that LB100, a small molecule inhibitor of PP2A, sensitizes cancer cells to radiation-mediated DNA damage. We hypothesized that LB100 could sensitize ovarian cancer cells to cisplatin treatment. We performed in vitro studies in SKOV-3, OVCAR-8, and PEO1, 4, and 6 ovarian cancer lines to assess cytotoxicity potentiation, cell-death mechanism(s), cell cycle regulation, and DNA damage response signaling. In vivo studies were conducted in an intraperitoneal metastatic mouse model using SKOV-3/f-Luc cells. LB100 sensitized ovarian carcinoma lines to cisplatin-mediated cell death. Sensitization via LB100 was mediated by abrogation of cell cycle arrest induced by cisplatin. Loss of the cisplatin-induced checkpoint correlated with decreased Wee1 expression, increased cdc2 activation, and increased mitotic entry (p-histone H3). LB100 also induced constitutive hyperphosphorylation of DNA damage response proteins (BRCA1, Chk2, ?H2AX), altered the chronology and persistence of JNK activation, and modulated the expression of 14-3-3 binding sites. In vivo, cisplatin sensitization via LB100 significantly enhanced tumor growth inhibition and prevented disease progression after treatment cessation. Our results suggest that LB100 sensitizes ovarian cancer cells to cisplatin in vitro and in vivo by modulation of the DNA damage response pathway and cell cycle checkpoint abrogation. �The Protein Phosphatase 2A Inhibitor LB100 Sensitizes Ovarian Carcinom(epmc).pdf DeepDyve Pubget Overpricing