The Potential of Epigallocatechin Gallate (EGCG) in Targeting Autophagy for Cancer Treatment: A Narrative Review

Int J Mol Sci. 2022 May 28;23(11):6075. doi: 10.3390/ijms23116075.

Abstract

Autophagy is an evolutionarily conserved process for the degradation of redundant or damaged cellular material by means of a lysosome-dependent mechanism, contributing to cell homeostasis and survival. Autophagy plays a multifaceted and context-dependent role in cancer initiation, maintenance, and progression; it has a tumor suppressive role in the absence of disease and is upregulated in cancer cells to meet their elevated metabolic demands. Autophagy represents a promising but challenging target in cancer treatment. Green tea is a widely used beverage with healthy effects on several diseases, including cancer. The bioactive compounds of green tea are mainly catechins, and epigallocatechin-gallate (EGCG) is the most abundant and biologically active among them. In this review, evidence of autophagy modulation and anti-cancer effects induced by EGCG treatment in experimental cancer models is presented. Reviewed articles reveal that EGCG promotes cytotoxic autophagy often through the inactivation of PI3K/Akt/mTOR pathway, resulting in apoptosis induction. EGCG pro-oxidant activity has been postulated to be responsible for its anti-cancer effects. In combination therapy with a chemotherapy drug, EGCG inhibits cell growth and the drug-induced pro-survival autophagy. The selected studies rightly claim EGCG as a valuable agent in cancer chemoprevention.

Keywords: autophagy; autophagy activator; autophagy modulator; cancer therapy; epigallocatechin gallate.

Publication types

  • Review

MeSH terms

  • Apoptosis
  • Autophagy
  • Catechin* / analogs & derivatives
  • Catechin* / pharmacology
  • Catechin* / therapeutic use
  • Humans
  • Neoplasms* / drug therapy
  • Phosphatidylinositol 3-Kinases
  • Tea

Substances

  • Tea
  • Catechin
  • epigallocatechin gallate

Grants and funding

This research received no external funding.