The Role of Isoflavones in the Prevention of Breast Cancer and Prostate Cancer

Abstract

This narrative review summarizes epidemiological studies on breast cancer and prostate cancer with an overview of their global incidence distribution to investigate the relationship between these diseases and diet. The biological properties, mechanisms of action, and available data supporting the potential role of isoflavones in the prevention of breast cancer and prostate cancer are discussed. Studies evaluating the effects of isoflavones in tissue cultures of normal and malignant breast and prostate cells, as well as the current body of research regarding the effects of isoflavones attained through multiple modifications of cellular molecular signaling pathways and control of oxidative stress, are summarized. Furthermore, this review compiles literature sources reporting on the following: (1) levels of estrogen in breast and prostate tissue; (2) levels of isoflavones in the normal and malignant tissue of these organs in European and Asian populations; (3) average concentrations of isoflavones in the secretion of these organs (milk and semen). Finally, particular emphasis is placed on studies investigating the effect of isoflavones on tissues via estrogen receptors (ER).

Keywords: breast cancer; isoflavones; prostate cancer.

Figure 1

Schematic representation of the phenolic compounds and their chemical structures.

Figure 2

Structures of isoflavones glycosides: daidzin, genistin and glycitin.

Figure 3

Graphical overview of the isoflavones’ possible molecular targets and cellular signaling pathways in the breast cancer model. Abbreviations: AKT, Protein kinase-B; Bcl-2, B-cell lymphoma 2; Bcl-xL, B-cell lymphoma-extra large; Bax, Bcl-2-associated X-protein; E2, Estradiol; EGF, epidermal growth factor; EGFR, Epidermal growth factor receptor; ERα, Estrogen receptor alpha; ERβ, Estrogen receptor beta; ERK, Extracellular-signal-regulated kinase; IGF, insulin-like growth factor; IGFR, insulin-like growth factor receptor; IKKα, IKKβ and IKKγ, IκB ki-nases; MAPK, Mitogen-activated protein kinases; MEK, Mitogen-activated protein kinase kinase; mTOR, mammalian target of rapamycin; NF-κB, nuclear factor-κB; PI3K, Phosphoinositide 3-kinase; PTEN, Phosphatase and tensin homolog; Raf, Rapidly accelerated fibrosarcoma; Ras, Rat sarcoma, TKR; Tyrosine kinase receptor.

Figure 4

Graphical overview of the isoflavones’ possible molecular targets and cellular signaling pathways in the prostate cancer model. Abbreviations: AKT, Protein kinase-B; AR, Androgen receptor; DHT, Dihydrotestosterone; E2, Estradiol; ERα, Estrogen receptor alpha; ERβ, Estrogen receptor beta; ERK, Extracellular-signal-regulated kinase; GPCR, G protein-coupled receptor; IKKα, IKKβ and IKKγ, IκB kinases; MEK, Mitogen-activated protein kinase kinase; mTOR, mammalian target of rapamycin; NF-κB, nuclear factor-κB; PI3K, Phosphoinositide 3-kinase; PTEN, Phosphatase and tensin homolog; Raf, Rapidly accelerated fibrosarcoma; Ras, Rat sarcoma; TKR, Tyrosine kinase receptor.