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Exploring the Complex Mechanisms of Isoflavones: From Cell Bioavailability, to Cell Dynamics and Breast Cancer
François Ferriere1, Nagham Aasi1, Gilles Flouriot1
1Université de Rennes, Inserm, EHESP, Irset (Institut de Recherche en Santé, Environnement et Travail) - UMR_S 1085, Rennes, France.
Abstract:
In Western countries, the increase in the consumption of soy-derived products raises the population's exposure to isoflavones. These molecules, present in many foods, have numerous effects on the body's cells, including regulation of the transcription and epigenetics, cell signaling, cell cycle, cell growth, apoptosis, and oxidative stress. However, despite the multitude of studies conducted, on these compounds, it remains difficult to draw definitive conclusions regarding their safety or dangerousness in the diet. Indeed, some epidemiological studies highlight health benefits in consuming isoflavone-rich foods, notably by reducing the risk of certain cancers. However, several studies conducted on cell models show that these molecules can have negative effects on cell fate, particularly with regard to proliferation and survival of mammary tumor cells. Isoflavones are mainly genistein, daidzein, formononetin, and biochanin A. These molecules belong to the family of phytoestrogens, which are capable of interacting with both nuclear estrogen receptor, ERα and ERβ, to trigger agonistic and antagonistic effects. Due to their estrogenic properties, isoflavones are suspected to promote hormone-dependent cancers such as breast cancer. This suspicion is based primarily on their ability to bind to ERα in breast cells, thereby altering the signaling pathways that control cell growth. However, study results are sometimes contradictory. Some studies suggest that isoflavones may protect against breast cancer by acting as selective estrogen receptor modulators, while others highlight their potential role in stimulating tumor growth. This review explores the literature on the effects of isoflavones, focusing on their influence on ERα-dependent signaling in breast tumor cells.
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