Calcineurin subunit B promotes TNF-alpha-induced apoptosis by binding to mitochondria and causing mitochondrial Ca2+ overload

被引：20

作者：

Cheng, Jinbo ^{[1
]}

Tang, Wei ^{[1
]}

Su, Zhenyi ^{[1
]}

Guo, Junxia ^{[1
]}

Tong, Li ^{[1
]}

Wei, Qun ^{[1
]}

机构：

[1] Beijing Normal Univ, Dept Biochem & Mol Biol, Beijing Key Lab, Beijing 100875, Peoples R China

来源：

CANCER LETTERS | 2012年 / 321卷 / 02期

基金：

中国国家自然科学基金;

关键词：

Calcineurin subunit B; TNF-alpha; Mitochondria; Ca2+ overload; BCL-2 FAMILY PROTEINS; ENDOPLASMIC-RETICULUM; CYTOCHROME-C; CELL-DEATH; RELEASE; ACTIVATION; CALCIUM; PRO-CASPASE-3; EXPRESSION; MATURATION;

D O I：

10.1016/j.canlet.2012.01.042

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Previous studies have shown that excess calcineurin subunit B (CnB) associates with mitochondria. Here, CnB overexpression increased CN activity in cells and enhanced TNF-alpha-induced cell death independent of CN activity. Overexpression of CnB increased intracellular Ca2+ concentration, enhanced caspase-3 activity, reduced Bcl-2 expression, and decreased mitochondrial membrane potential, with no change of caspase-8 or p53. CnB bound to isolated mitochondria in a Ca2+-dependent manner, and stimulated cytochrome c release from the mitochondria. Altogether, these results demonstrate that CnB is capable of promoting TNF-alpha-induced apoptosis, possibly through effects on mitochondrial functions. (c) 2012 Elsevier Ireland Ltd. All rights reserved.

引用

页码：169 / 178

页数：10

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