AKAP12 induces apoptotic cell death in human fibrosarcoma cells by regulating CDKI-cyclin D1 and caspase-3 activity

被引：43

作者：

Yoon, Dae-Kwan ^{[1
]}

Jeong, Chul-Ho ^{[1
]}

Jun, Hyoung Oh ^{[1
]}

Chun, Kwang-Hoon ^{[1
]}

Cha, Jong-Ho ^{[1
]}

Seo, Ji Hae ^{[1
]}

Lee, Hae Young ^{[1
]}

Choi, Yoon Kyung ^{[1
]}

Ahn, Bum-Ju ^{[1
]}

Lee, Seung-Ki ^{[1
]}

Kim, Kyu-Won ^{[1
]}

机构：

[1] Seoul Natl Univ, Coll Pharm, Res Inst Pharmaceut, Div Pharmaceut Biosci,NeuroVasc Coordinat Res Ctr, Seoul 151742, South Korea

来源：

CANCER LETTERS | 2007年 / 254卷 / 01期

关键词：

AKAP12; apoptosis; cell cycle arrest; cyclin D1; caspase-3;

D O I：

10.1016/j.canlet.2007.02.017

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

AKAP12 (A-Kinase anchoring protein 12) is a protein kinase C substrate and a potential tumor suppressor. AKAP12 is down-regulated by several oncogenes and strongly suppressed in various cancers including prostate, ovarian and breast cancers. AKAP12 acts as a regulator of mitogenesis by anchoring key signal proteins such as PKA, PKC, and cyclins. In this study, AKAP12 was found to suppress tumor cell viability by inducing apoptosis via caspase-3 in HT1080 cells. This AKAP12-induced apoptosis was associated with a decreased expression of Bcl-2 and increased expression of Bax. Moreover, AKAP12-transfectant strongly induced the expression of Cip1/p21 and Kip1/p27, but resulted in a decrease in cyclin D1 involved in G(1) progression. Accordingly, these results suggest that AKAP12 may play an important role in tumor growth suppression by inducing apoptosis with the regulation of multiple molecules in the cell cycle progression. (c) 2007 Published by Elsevier Ireland Ltd.

引用

页码：111 / 118

页数：8

共 20 条

[1] CYCLIN D1 IS A NUCLEAR-PROTEIN REQUIRED FOR CELL-CYCLE PROGRESSION IN G(1) [J].