PI 3-kinase/Akt and STAT3 are required for the prevention of TGF-β-induced Hep3B cell apoptosis by autocrine motility factor/phosphoglucose isomerase

被引：19
|
作者：
Shih, Wen-Ling [1 ]
Liao, Ming-Huei [2 ]
Lin, Ping-Yuan [3 ]
Chang, Chi-I [1 ]
Cheng, Hsueh-Ling [1 ]
Yu, Feng-Ling [4 ]
Lee, Jeng-Woei [3 ]
机构：
[1] Natl Pingtung Univ Sci & Technol, Grad Inst Biotechnol, Neipu 91201, Pingtung, Taiwan
[2] Natl Pingtung Univ Sci & Technol, Dept Vet Med, Neipu 91201, Pingtung, Taiwan
[3] Tzu Chi Univ, Grad Inst Life Sci, Hualien, Taiwan
[4] Tzu Hui Inst Technol, Dept Nursing, Pingtung, Taiwan
来源：
CANCER LETTERS | 2010年 / 290卷 / 02期
关键词：
AMF/PGI; TGF-beta; PI; 3-kinase; Akt; STAT3; PHOSPHATIDYLINOSITOL; 3-KINASE; PHOSPHOGLUCOSE ISOMERASE; UP-REGULATION; PROTEIN; ACTIVATION; SURVIVAL; DEATH; RECEPTOR; BINDING; GENE;
D O I：
10.1016/j.canlet.2009.09.014
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
We established Hep3B cells stably-expressing wild-type and mutated AMF/PGI with differing enzymatic activities in order to investigate how AMF/PGI affects TGF-beta-induced apoptosis, and demonstrated that AMF/PGI against TGF-beta-induced apoptosis was correlated with its enzymatic activity. AMF/PGI did not alter TGF-beta-receptor expression nor affect TGF-beta-induced PAI-1 gene promoter or Smad3/4 activity. AMF/PGI induced PI 3-kinase activity, IRS and Akt phosphorylation, which can further regulate BAD phosphorylation. Constitutively-active p110 enhanced AMF/PGI-mediated anti-apoptosis activity, and dominant negative Akt alleviated anti-TGF-beta-induced apoptosis. We also demonstrated that STAT3 is a weak anti-apoptotic agent but has an increased anti-apoptotic effect in cooperation with PI 3-kinase/Akt. Crown Copyright (C) 2009 Published by Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：223 / 237
页数：15
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