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10.1158/2159-8290.CD-14-1113 http://scihub22266oqcxt.onion/10.1158/2159-8290.CD-14-1113 C4456272!4456272!25829425     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25829425&cmd=llinks): Failed to open stream: HTTP request failed! 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Myc drives Pten/p53-deficient proliferation and metastasis due to Il6-secretion and Akt-suppression via Phlpp2 |pdf=|usr=}}{{25829425}} gab.com Text Myc drives Pten/p53-deficient proliferation and metastasis due to Il6-secretion and Akt-suppression via Phlpp2 JO: Cancer Discov http://www.kidney.de/pget.php?&tw=1&pmid=25829425 #FOAvip We have recently recapitulated metastasis of human PTEN/TP53-mutant PC in mouse using the RapidCaP system. Surprisingly, we found that this metastasis is driven by Myc-, and not Akt-activation.Here, we show that cell-cell communication by Il6 drives the Akt-Myc switch through activation of the Akt-suppressing phosphatase Phlpp2, when Pten and p53 are lost together, but not separately. Il6 then communicates a downstream program of Stat3-mediated Myc-activation, which drives cell proliferation. Similarly in tissues, peak proliferation in Pten/Trp53 mutant primary and metastatic PC does not correlate with activated Akt, but with Stat3/Myc activation instead. Mechanistically, Myc strongly activates the Akt phosphatase Phlpp2 in primary cells and PC metastasis. We show genetically that Phlpp2 is essential for dictating proliferation of Myc-mediated Akt-suppression.Collectively, our data reveal competition between two proto-oncogenes: Myc and Akt, which ensnarls the Phlpp2 gene to facilitate Myc-driven PC metastasis after loss of Pten and Trp53. Twit Text FOAVip Myc drives Pten/p53-deficient proliferation and metastasis due to Il6-secretion and Akt-suppression via Phlpp2 ????Cancer Discov http://www.kidney.de/pget.php?&tw=1&pmid=25829425 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25829425 #FOAvip English Wikipedia <ref>{{Cite pmid|25829425}}</ref> Myc drives Pten/p53-deficient proliferation and metastasis due to Il6-secretion and Akt-suppression via Phlpp2 #MMPMID25829425 Nowak DG; Cho H; Herzka T; Watrud K; DeMarco DV; Wang VMY; Senturk S; Fellmann C; Ding D; Beinortas T; Kleinman D; Chen M; Sordella R; Wilkinson JE; Castillo-Martin M; Cordon-Cardo C; Robinson BD; Trotman LC Cancer Discov 2015[Jun]; 5 (6): 636-51 PMID25829425show ga We have recently recapitulated metastasis of human PTEN/TP53-mutant PC in mouse using the RapidCaP system. Surprisingly, we found that this metastasis is driven by Myc-, and not Akt-activation.Here, we show that cell-cell communication by Il6 drives the Akt-Myc switch through activation of the Akt-suppressing phosphatase Phlpp2, when Pten and p53 are lost together, but not separately. Il6 then communicates a downstream program of Stat3-mediated Myc-activation, which drives cell proliferation. Similarly in tissues, peak proliferation in Pten/Trp53 mutant primary and metastatic PC does not correlate with activated Akt, but with Stat3/Myc activation instead. Mechanistically, Myc strongly activates the Akt phosphatase Phlpp2 in primary cells and PC metastasis. We show genetically that Phlpp2 is essential for dictating proliferation of Myc-mediated Akt-suppression.Collectively, our data reveal competition between two proto-oncogenes: Myc and Akt, which ensnarls the Phlpp2 gene to facilitate Myc-driven PC metastasis after loss of Pten and Trp53. äMyc drives Pten/p53-deficient proliferation and metastasis due to Il6-(epmc).pdf DeepDyve Pubget Overpricing