Induction of apoptosis by epigallocatechin-3-gallate via mitochondrial signal transduction pathway

被引：34

作者：

Zhao, Y ^{[1
]}

Yang, LF ^{[1
]}

Ye, M ^{[1
]}

Gu, HH ^{[1
]}

Cao, Y ^{[1
]}

机构：

[1] Cent S Univ, Xiangya Sch Med, Canc Res Inst, Changsha 410078, Hunan, Peoples R China

来源：

PREVENTIVE MEDICINE | 2004年 / 39卷 / 06期

基金：

中国国家自然科学基金;

关键词：

tea polyphenols; EGCG; Epstein-Barr virus; latent membrane protein 1; nasopharyngeal neoplasms; mitochondria; caspase;

D O I：

10.1016/j.ypmed.2004.04.042

中图分类号：

R1 [预防医学、卫生学];

学科分类号：

1004 ; 120402 ;

摘要：

Purpose. To elucidate the apoptosis induction of Epigallocatechin-3-gallate (EGCG) on nasopharyngeal carcinoma (NPC) cells via mitochondrial signal transduction pathway regulated by EB-virus-encoded latent membrane protein 1 (LMP1). Methods. The survival rates of pTet-on-LMP1 HNE2 cells after the EGCG treatment were determined by MTT assay. Induction of apoptosis in pTet-on-LMP1 HNE2 cells after the EGCG treatment was analyzed by agarose gel electrophoresis. The activity of caspase-9 was determined by ApoAlert Caspase-9 Fluorescent Assay kit after the EGCG treatment. The protein expressions of cytochrome c and Bcl-2 were analyzed by Western blotting after the EGCG treatment. Results. EGCG inhibited the survival rates of pTet-on-LMP1 HNE2 cells and induced apoptosis of pTet-on-LMP1 HNE2 cells. EGCG raised the activities of caspase-9, enhanced the releasing of cytochrome c from the mitochondria, and suppressed the protein expression of Bcl-2. These are the key targets on the mitochondrial signal transduction pathway in apoptosis. Conclusions. EGCG inhibited the survival rate of NPC cells and induced apoptosis of NPC cells via the mitochondrial signal transduction pathway. This study suggests that the interference effect of EGCG on targets of the mitochondrial signal transduction pathway plays an important role in the anticancer function. (C) 2004 The Institute For Cancer Prevention and Elsevier Inc. All rights reserved.

引用

页码：1172 / 1179

页数：8

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