Involvement of AMPK signaling cascade in capsaicin-induced apoptosis of HT 29 colon cancer cells

被引:85
|
作者
Kim, Young Min
Hwang, Jin-Taek
Kwak, Dong Wook
Lee, Yun Kyung
Park, Ock Jin [1 ]
机构
[1] Hannam Univ, Dept Food & Nutr, Taejon 306791, South Korea
[2] Hannam Univ, Dept Biol Sci, Taejon 306791, South Korea
[3] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02114 USA
来源
SIGNAL TRANSDUCTION PATHWAYS, PT C: CELL SIGNALING IN HEALTH AND DISEASE | 2007年 / 1095卷
关键词
cell death; capsaicin; AMPK; AICAR; HT-29; cells;
D O I
10.1196/annals.1397.053
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Adenosine monophosphate (AMP)-activated protein kinase (AMPK) is activated during ATP-depleting metabolic states, such as hypoxia, heat shock, oxidative stress, and exercise. As a highly conserved heterotrimeric kinase that functions as a major metabolic switch to maintain energy homeostasis, AMPK has been shown to exert as an intrinsic regulator of mammalian cell cycle. Moreover, AMPK cascade has emerged as an important pathway implicated in cancer control. In this article, we have investigated the effects of capsaicin on apoptosis in relation to AMPK activation in colon cancer cell. Capsaicin-induced apoptosis was revealed by the presence of nucleobodies in the capsaicin-treated HT-29 colon cancer cells. Concomitantly, the activation of AMPK and the increased expression of the inactive form of acetyl-CoA carboxylase (ACC) were detected in capsaicin-treated colon cancer cells. We showed that both capsaicin and 5'-aminoimidazole-4-carboxamide-1-beta-D-ribonucleoside (AICAR), an AMPK activator possess the AMPK-activating capacity as well as apoptosis-inducing properties. Evidence of the association between AMPK activation and the increased apoptosis in HT 29 colon cancer cells by capsaicin treatment, and further findings of the correlation of the activated AMPK and the elevated apoptosis by cotreatment of AICAR and capsaicin support AMPK as an important component of apoptosis, as well as a possible target of cancer control.
引用
收藏
页码:496 / 503
页数:8
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