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J Steroid Biochem Mol Biol. 2014 Mar;140:116-32. doi: 10.1016/j.jsbmb.2013.12.010. Epub 2013 Dec 25.

Soy isoflavones and prostate cancer: a review of molecular mechanisms.

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Department of Pathology, University of Illinois at Chicago, Chicago, IL, USA. Electronic address:
Department of Pathology, University of Illinois at Chicago, Chicago, IL, USA; Department of Pathology, Xinxiang Medical University, Xinxiang, China.
Department of Pathology, University of Illinois at Chicago, Chicago, IL, USA.


Soy isoflavones are dietary components for which an association has been demonstrated with reduced risk of prostate cancer (PCa) in Asian populations. However, the exact mechanism by which these isoflavones may prevent the development or progression of PCa is not completely understood. There are a growing number of animal and in vitro studies that have attempted to elucidate these mechanisms. The predominant and most biologically active isoflavones in soy products, genistein, daidzein, equol, and glycetin, inhibit prostate carcinogenesis in some animal models. Cell-based studies show that soy isoflavones regulate genes that control cell cycle and apoptosis. In this review, we discuss the literature relevant to the molecular events that may account for the benefit of soy isoflavones in PCa prevention or treatment. These reports show that although soy isoflavone-induced growth arrest and apoptosis of PCa cells are plausible mechanisms, other chemo protective mechanisms are also worthy of consideration. These possible mechanisms include antioxidant defense, DNA repair, inhibition of angiogenesis and metastasis, potentiation of radio- and chemotherapeutic agents, and antagonism of estrogen- and androgen-mediated signaling pathways. Moreover, other cells in the cancer milieu, such as the fibroblastic stromal cells, endothelial cells, and immune cells, may be targeted by soy isoflavones, which may contribute to soy-mediated prostate cancer prevention. In this review, these mechanisms are discussed along with considerations about the doses and the preclinical models that have been used.


APC; APE1/Ref; APK; B-cell translocation gene; BTG; CSC; CSF; Chemoprevention; DSH; ECGF1; EPHB; FAK; GADD; GM-CSF; GPx; GSK3β; GSR; GSTP; GSk-3β; Genistein; HAT; Isoflavone; LEF; LHRH; N-benzyloxycarbonyl-Val-Asp-fluoromethyl-ketone; Prostate cancer; RASSF; TAMs; TRIM; activated protein kinase; adenomatous polyposis coli; apurinic apyrimidinic endonuclease redox effector factor; cancer stem cells; colony-stimulating factor; disheveled; endothelial cell growth factor; ephrin B; focal adhesion kinase; glutathione S-transferase P; glutathione peroxidase; glutathione reductase; glycogen synthase kinase 3β; glycogen synthase kinase-3β; granulocyte monocyte-colony stimulating factor; growth arrest and DNA damage; histone acetyltransferases; luteinizing hormone releasing hormone; lymphoid enhancer factor; ras association domain family; tripartite motif-containing protein; tumor associated macrophages; uPA; urokinase-type plasminogen activator; z-VAD-fmk

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