Curcumin, a polyphenolic compound derived from turmeric (Curcuma longa Linn), possesses remarkable medicinal properties and has been extensively studied over four decades for its potential anti-inflammatory and/or anticancer effects. The epigenetic impact of curcumin in cancer prevention is yet largely an unexplored area of research, with sporadic reports of its epigenetic modulatory properties. Epigenetics represents an evolving strategy for cancer chemoprevention and has been established as a promising approach in human clinical trials. Epigenetic studies include DNA methylation, histone lysine acetylation/deacetylation, histone methylation/demethylation, and arginine methylation. These epigenetic changes are mediated by specific enzymes, such as lysine acetyltransferases/deacetylases and lysine methyltransferases/demethylases, which regulate this reversible posttranslational modification as well as nuclear transcriptional processes. Curcumin has been reported to modulate epigenetic changes in cancer cells; however, this preventive aspect has not been much reported. Curcumin has been shown to be a DNA hypomethylation agent in colon, prostate, and breast cancer, thus serving as a chemopreventive agent. Among these curcumin-induced epigenetic alterations is modulation of the expression of several oncogenic and tumor-suppressor microRNAs (miRs). Suppression of oncomiRs, such as miR-21, miR-17-5p, miR-20a, and miR-27a, and overexpression of miR-34 a/c and epithelial-mesenchymal transition-suppressor miRs, are among the most important effects of curcumin on miRs homeostasis. The present chapter is designed to collate the existing literature and comprehensively discuss the current understanding of potential epigenetic targets of curcumin and its effects on cancer chemoprevention.
|Name||Translational Epigenetics Series|