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The Epigenetic Modification of Epigallocatechin Gallate (EGCG) on Cancer.

Abstract
Among the major components of green tea, epigallocatechin-3-gallate (EGCG) is the most effective for its anti-cancer characteristics. The bulk of studies provide the mechanisms of suppressive function of EGCG are involved in alteration of cancer cell cycle, development, and apoptosis through activation/inhibition of several signal pathways. Another mechanism that explains the multiple effects exerted by EGCG in cancer is the epigenetic change by DNA methylation or methyltransferases, histone acetylation or deacetylases, and no coding RNAs (micoRNAs). Furthermore, decontrolled expression of miRNA transcription has been tested to be directly regulated by oncogenic and tumor-suppressor transcription factors. Recently, several proteins have been identified as miRNA direct interactors by EGCG. However, the mechanisms explaining the action of miRNA being modulated by EGCG have not been completely understood yet. This review summarizes the state of epigenetic change being modulated by EGCG in a variety of cancers and oncogenic and tumor-suppressor transcription factors.
AuthorsLinqi Yang, Wenqi Zhang, Saiyam Chopra, Deeepjyot Kaur, Huibing Wang, Meng Li, Pingping Chen, Wei Zhang
JournalCurrent drug targets (Curr Drug Targets) Vol. 21 Issue 11 Pg. 1099-1104 ( 2020) ISSN: 1873-5592 [Electronic] United Arab Emirates
PMID32364072 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
CopyrightCopyright© Bentham Science Publishers; For any queries, please email at [email protected].
Chemical References
  • Anticarcinogenic Agents
  • Histone Deacetylase Inhibitors
  • MicroRNAs
  • Catechin
  • epigallocatechin gallate
  • DNA Modification Methylases
Topics
  • Anticarcinogenic Agents (pharmacology, therapeutic use)
  • Catechin (analogs & derivatives, pharmacology, therapeutic use)
  • Cell Line, Tumor
  • DNA Modification Methylases (antagonists & inhibitors)
  • Epigenesis, Genetic (drug effects)
  • Histone Deacetylase Inhibitors (therapeutic use)
  • Humans
  • MicroRNAs (drug effects, genetics)
  • Neoplasms (drug therapy, genetics, metabolism)

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