Bcl-2 blocks apoptotic signal of transforming growth factor-β in human hepatoma cells

被引：18

作者：

Huang, YL

Chou, CK ^{[1
]}

机构：

[1] Vet Gen Hosp, Dept Med Res, Taipei 112, Taiwan

[2] Natl Yang Ming Univ, Inst Biochem, Taipei 112, Taiwan

[3] Natl Hlth Res Inst, Div Mol & Genom Med, Taipei, Taiwan

来源：

JOURNAL OF BIOMEDICAL SCIENCE | 1998年 / 5卷 / 03期

关键词：

TGF-beta; Bcl-2; apoptosis; antioxidative enzyme; reactive oxygen species;

D O I：

暂无

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Transforming growth factor-beta (TGF-beta) has been shown to induce apoptosis on normal hepatocytes and hepatoma cells both in vitro and in vivo. However, how the TGF-beta induces apoptosis is still not clear. We examined the expression of anti-apoptosis proteins and sensitivity to TGF-beta in three well differentiated human hepatoma cell lines. Two TGF-beta sensitive cell lines Hep3B and HuH7 totally lacked Bcl-2. In contrast, the TGF-beta resistant HepG2 cells expressed a substantial amount of Bcl-2. AU three cell lines expressed equal amounts of Bcl-X-L, Bcl-X-S and Bar. Overexpression of Bcl-2 in Hep3B and HuH7 cells protected them from TGF-beta-induced apoptosis. TGF-beta treatment increased intracellular peroxide production and suppressed the expression of glutathione-S-transferase in the Hep3B cells, and these effects were partially suppressed by the overexpression of Bcl-2. These results suggest that Bcl-2 may protect cell from TGF-beta-F-induced apoptosis by interfering TGF-beta generated signals leading to induce reactive oxygen species production.

引用

页码：185 / 191

页数：7

共 59 条

[1]

AKAO Y, 1994, CANCER RES, V54, P2468

[2] THE PROTOONCOGENE BCL-2 CAN SELECTIVELY RESCUE NEUROTROPHIC FACTOR-DEPENDENT NEURONS FROM APOPTOSIS [J].