Epigenetics of breast cancer: Modifying role of environmental and bioactive food compounds

Abstract

Scope Reduced expression of tumor suppressor genes (TSG) increases the susceptibility to breast cancer. However, only a small percentage of breast tumors is related to family history and mutational inactivation of TSG. Epigenetics refers to non-mutational events that alter gene expression. Endocrine disruptors found in foods and drinking water may disrupt epigenetically hormonal regulation and increase breast cancer risk. This review centers on the working hypothesis that agonists of the aromatic hydrocarbon receptor (AHR); bisphenol A (BPA); and arsenic compounds, induce in TSG epigenetic signatures that mirror those often seen in sporadic breast tumors. Conversely, it is hypothesized that bioactive food components that target epigenetic mechanisms protect against sporadic breast cancer induced by these disruptors. Methods and results This review highlights 1) overlaps between epigenetic signatures placed in TSG by AHR-ligands, BPA, and arsenic with epigenetic alterations associated with sporadic breast tumorigenesis; and 2) potential opportunities for prevention of sporadic breast cancer with food components that target the epigenetic machinery. Conclusions Characterizing the overlap between epigenetic signatures elicited in TSG by endocrine disruptors with those observed in sporadic breast tumors may afford new strategies for breast cancer prevention with specific bioactive food components or diet.

FEN1 mediates miR‐200a methylation and promotes breast cancer cell growthviaMET and EGFR signaling

“…Aberrant DNA methylation is known to lead to numerous human diseases. In breast cancer, hypermethylation of BRCA1, ESR1, CDH1, and APC-or hypomethylation of MUC1 and Let-7a-have been frequently observed (38,39). Most of the studies have focused on genes' aberrant methylation, whereas the regulation mechanisms of methylation are poorly understood.…”

Perfluorinated alkylated substances serum concentration and breast cancer risk: Evidence from a nested case‐control study in the French E3N cohort

“…On this regard, a list of EDCs has exhibited strong effects on the development of mammary glands, prompting the hypothesis of potential effects on BC pathogenesis . It has also been suggested that several EDCs lead to epigenetic changes that can in turn induce altered gene function and malignant cellular transformation . However, despite the biological plausibility of a strong influence of endogenous estrogens and androgens on BC, the potential involvement of EDCs in the development of BC remains to be confirmed …”

“…5 It has also been suggested that several EDCs lead to epigenetic changes that can in turn induce altered gene function and malignant cellular transformation. 6 However, despite the biological plausibility of a strong influence of endogenous estrogens and androgens on BC, the potential involvement of EDCs in the development of BC remains to be confirmed. 7 Perfluorinated alkylated substances (PFASs) constitute a family of environmental EDCs, for which the long-term health effects are uncharacterized in terms of their relation to BC risk.…”

Dioscin induces demethylation of DAPK-1 and RASSF-1alpha genes via the antioxidant capacity, resulting in apoptosis of bladder cancer T24 cells

“…There is evidence that modern lifestyles have strong association with the high incident of BC, which can induce epigenetic transformation, resulting in aberrant expression of some cancer-related genes (Romagnolo et al, 2016[7]; Shankar et al, 2016[9]). Epigenetic control of gene transcription includes methylation of the DNA and covalent modifications, such as acetylation and methylation, of chromatin's histone proteins.…”