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. 2012 Jun;1(2):78-88.
doi: 10.3978/j.issn.2223-4683.2012.05.06.

TGF-β mediated DNA methylation in prostate cancer

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TGF-β mediated DNA methylation in prostate cancer

Chung Lee et al. Transl Androl Urol. 2012 Jun.

Abstract

Almost all tumors harbor a defective negative feedback loop of signaling by transforming growth factor-β (TGF-β). Epigenetic mechanisms of gene regulation, including DNA methylation, are fundamental to normal cellular function and also play a major role in carcinogenesis. Recent evidence demonstrated that TGF-β signaling mediates cancer development and progression. Many key events in TGF-β signaling in cancer included auto-induction of TGF-β1 and increased expression of DNA methyltransferases (DNMTs), suggesting that DNA methylation plays a significant role in cancer development and progression. In this review, we performed an extensive survey of the literature linking TGF-β signaling to DNA methylation in prostate cancer. It appeared that almost all DNA methylated genes detected in prostate cancer are directly or indirectly related to TGF-β signaling. This knowledge has provided a basis for our future directions of prostate cancer research and strategies for prevention and therapy for prostate cancer.

Keywords: DNA methylation; DNMT; Erk activation; TGF-β; prostate cancer; tumor development and progression.

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Conflict of interest statement

Conflicts of Interest: M. McClelland and D. Mercola are cofounders Proveri Inc., which is engaged in translational development of aspects of the subject matter. The other authors have no conflicts of interest to declare.

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References

    1. Mu Y, Gudey SK, Landström M. Non-Smad signaling pathways. Cell Tissue Res 2012;347:11-20. - PubMed
    1. Yu N, Kozlowski JM, Park II, et al. Over-expression of transforming growth factor 1 in malignant prostate cells is partly caused by a runaway of TGF-1 auto-induction mediated through a defective recruitment of protein phosphatase 2A by TGF-type I receptor. Urology 2010;76:1519.e8-13. - PMC - PubMed
    1. Zhang Q, Chen L, Helfand BT, et al. Transforming Growth Factor-â-induced DNA methyltransferase contributes to aggressive prostate cancer phenotypes and predicts biochemical recurrence after radical prostatectomy. PLoS ONE 2011;6:e25168. - PubMed
    1. Nelson WG, De Marzo AM, Yegnasubramanian S. Epigenetic alterations in human prostate cancers. Endocrinology 2009;150:3991-4002. - PMC - PubMed
    1. Phé V, Cussenot O, Rouprêt M. Methylated genes as potential biomarkers in prostate cancer. BJU Int 2010;105:1364-70. - PubMed