In:
Annals of the New York Academy of Sciences, Wiley, Vol. 1171, No. 1 ( 2009-08), p. 538-544
Abstract:
This study investigated the apoptotic regulation by green tea catechin epigallcatechin‐3‐gallate (EGCG) on colon cancer cells in the presence of low‐dose H 2 O 2 known to exert the activation of signal pathways leading to cell proliferation. In the presence of low‐dose H 2 O 2 , EGCG induced apoptosis and abolished the cell‐proliferative effect exhibited by low‐dose H 2 O 2 . This reduction of growth was accompanied by an activation of AMP‐activated kinase (AMPK), a decrease in cyclooxygenase‐2 (COX‐2) expression and prostaglandin E 2 (PGE 2 ) levels, and the induction of apoptotic markers such as p53 and poly(ADP‐ribose) polymerase (PARP) cleavage. The low‐dose H 2 O 2 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 PGE 2 . 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 H 2 O 2 .
Type of Medium:
Online Resource
ISSN:
0077-8923
,
1749-6632
DOI:
10.1111/nyas.2009.1171.issue-1
DOI:
10.1111/j.1749-6632.2009.04698.x
Language:
English
Publisher:
Wiley
Publication Date:
2009
detail.hit.zdb_id:
2834079-6
detail.hit.zdb_id:
211003-9
detail.hit.zdb_id:
2071584-5
SSG:
11