Dietary molecules and experimental evidence of epigenetic influence in cancer chemoprevention: An insight

• Published in: Seminars in cancer biology 2022-08, Vol.83, p.319-334
• Main Authors: Ullah, Mohammad Fahad, Usmani, Shazia, Shah, Aaliya, Abuduhier, Faisel M.
• Format: Article
• Language: English
• Subjects: Cancer chemoprevention; Dietary factors; Epigenetic therapy; Non-coding RNAs; Signaling pathways
• ISSN: 1044-579X; 1096-3650
• DOI: 10.1016/j.semcancer.2020.10.011

The world-wide rate of incidence of cancer disease has been only modestly contested by the past and current preventive and interventional strategies. Hence, the global effort towards novel ideas to contain the disease still continues. Constituents of human diets have in recent years emerged as key regulators of carcinogenesis, with studies reporting their inhibitory potential against all the three stages vis-a-vis initiation, promotion and progression. Unlike drugs which usually act on single targets, these dietary factors have an advantage of multi-targeted effects and pleiotropic action mechanisms, which are effective against cancer that manifest as a micro-evolutionary and multi-factorial disease. Since most of the cellular targets have been identified and their consumption considered relatively safe, these diet-derived agents often appear as molecules of interest in repurposing strategies. Currently, many of these molecules are being investigated for their ability to influence the aberrant alterations in cell’s epigenome for epigenetic therapy against cancer. Targeting the epigenetic regulators is a new paradigm in cancer chemoprevention which acts to reverse the warped-up epigenetic alterations in a cancer cell, thereby directing it towards a normal phenotype. In this review, we discuss the significance of dietary factors and natural products as chemopreventive agents. Further, we corroborate the experimental evidence from existing literature, reflecting the ability of a series of such molecules to act as epigenetic modifiers in cancer cells, by interfering with molecular events that map the epigenetic imprints such as DNA methylation, histone acetylation and non-coding RNA mediated gene regulation.