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Modulatory role of tea in arsenic induced epigenetic alterations in carcinogenesis

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Abstract

Epigenetic alterations, broadly divided into DNA methylation, Histone modifications and interference by non-coding RNAs can often lead to carcinogenesis. Alterations in epigenetic machinery may be due to numerous factors, including exposure to toxic chemicals. These toxicants include heavy metals as well. The metalloid arsenic is an environmental pollutant and its chronic exposure causes cancer. Etiology of arsenic induced cancer includes epigenetic alterations, among others. Inorganic-arsenic is the lead cause of hypermethylation of tumor-suppressor genes and hypomethylation of genes involved in cell proliferation, growth and invasion. It can induce histone methylations and acetylations along with modulation of miRNAs, promoting cancer. Therefore, control of epigenetic alterations is vital. Chemoprevention using phytochemicals is an effective strategy to mitigate the deleterious effect of chronic arsenic exposure. Flavonoids, a group of phytochemicals have shown numerous evidences of epigenetic modulations halting carcinogenesis. Catechins represent one of the most active groups of flavonoids. Tea, a popular beverage, is one of the richest sources of catechins. Green tea contains highly active catechins like epigallocatechin-3-gallate (EGCG), epigallocatechin (EGC), epicatechingallate (ECG) etc. while black tea contains oxidized polymeric catechins like theaflavin and thearubigin. Green tea catechins have elicited their potential as an epigenetic modulator, establishing their chemopreventive attributes. Therefore, administration of tea may be an effective strategy to mitigate the epigenetic alterations, induced by chronic exposure to arsenic, in individuals of endemic areas.

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Acknowledgement

Authors are indebted to Director, Chittaranjan National Cancer Institute, Kolkata, India for providing infrastructural support and fellowship to AG.

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Ghosh, A., Mukherjee, S., Roy, M. et al. Modulatory role of tea in arsenic induced epigenetic alterations in carcinogenesis. Nucleus 64, 143–156 (2021). https://doi.org/10.1007/s13237-020-00346-9

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