JimJimJimJim Posted August 8, 2014 Share Posted August 8, 2014 Jim Marshall (not a doctor) said ... Genistein, a component of soy, is sometimes added to alternative medicines for prostate cancer. It is a type of chemical called a phytoestrogen. It may protect against getting prostate cancer in the first place. But this paper reports the bad news that once your prostate cancer gets more advanced, genistein may help it to grow faster. An unusual feature of the drug's activity is that it made cancers grow faster in the lab at concentrations our bodies can take (physiological doses), but slowed the cancers in the lab at higher doses than our bodies can take. ... end Jim PLoS One. 2013 Oct 22;8(10):e78479. doi: 10.1371/journal.pone.0078479. eCollection 2013. Differential effects of genistein on prostate cancer cells depend on mutational status of the androgen receptor. Mahmoud AM1, Zhu T, Parray A, Siddique HR, Yang W, Saleem M, Bosland MC. Author information Abstract Blocking the androgen receptor (AR) activity is the main goal of therapies for advanced prostate cancer (PCa). However, relapse with a more aggressive, hormone refractory PCa arises, which harbors restored AR activity. One mechanism of such reactivation occurs through acquisition of AR mutations that enable its activation by various steroidal and non-steroidal structures. Thus, natural and chemical compounds that contribute to inappropriate (androgen-independent) activation of the AR become an area of intensive research. Here, we demonstrate that genistein, a soy phytoestrogen binds to both the wild and the Thr877Ala (T877A) mutant types of AR competitively with androgen, nevertheless, it exerts a pleiotropic effect on PCa cell proliferation and AR activity depending on the mutational status of the AR. Genistein inhibited, in a dose-dependent way, cell proliferation and AR nuclear localization and expression in LAPC-4 cells that have wild AR. However, in LNCaP cells that express the T877A mutant AR, genistein induced a biphasic effect where physiological doses (0.5-5 µmol/L) stimulated cell growth and increased AR expression and transcriptional activity, and higher doses induced inhibitory effects. Similar biphasic results were achieved in PC-3 cells transfected with AR mutants; T877A, W741C and H874Y. These findings suggest that genistein, at physiological concentrations, potentially act as an agonist and activate the mutant AR that can be present in advanced PCa after androgen ablation therapy. PMID: 24167630 This extract can be found on http://PubMed.com, and is in the public domain. On PubMed.com there will be a link to the full paper (often $30, sometimes free). Any highlighting (except the title) is not by the author, but by Jim Marshall. Jim is not a doctor. Link to comment Share on other sites More sharing options...
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