Green Tea Catechin Controls Apoptosis in Colon Cancer Cells by Attenuation of H2O2-Stimulated COX-2 Expression via the AMPK Signaling Pathway at Low-Dose H2O2.

This study investigated the apoptotic regulation by green tea catechin epigallcatechin-3-gallate (EGCG) on colon cancer cells in the presence of low-dose H₂O₂ known to exert the activation of signal pathways leading to cell proliferation. In the presence of low-dose H₂O₂, EGCG induced apoptosis and abolished the cell-proliferative effect exhibited by low-dose H₂O₂. This reduction of growth was accompanied by an activation of AMP-activated kinase (AMPK), a decrease in cyclooxygenase-2 (COX-2) expression and prostaglandin E₂ (PGE₂) levels, and the induction of apoptotic markers such as p53 and poly(ADP-ribose) polymerase (PARP) cleavage. The low-dose H₂O₂ stimulated COX-2 expression, and treating cells with synthetic AMPK activator AICAR (5-aminoimiazole-4-carboxamide-1-β-d-ribofuranoside) resulted in greater suppression of COX-2 expression and PGE₂. By treating cells with high concentrations of the reactive oxygen species (ROS) scavenger NAC ( N-acetyl-1-cysteine), the apoptotic effect of EGCG was abolished and led to suppression of AMPK and COX-2, indicating that the liberation of excessive ROS might be the upstream signal of the AMPK–COX-2 signaling pathway even in the presence of low-dose H₂O₂. [ABSTRACT FROM AUTHOR]