Mice lacking a transcriptional corepressor Tob are predisposed to cancer

被引：103

作者：

Yoshida, Y

Nakamura, T

Komoda, M

Satoh, H

Suzuki, T

Tsuzuku, JK

Miyasaka, T

Yoshida, EH

Umemori, H

Kunisaki, RK

Tani, K

Ishii, S

Mori, S

Suganuma, M

Noda, T

Yamamoto, T ^{[1
]}

机构：

[1] Univ Tokyo, Inst Med Sci, Div Oncol, Minato Ku, Tokyo 1088639, Japan

[2] Univ Tokyo, Inst Med Sci, Div Pathol, Minato Ku, Tokyo 1088639, Japan

[3] Univ Tokyo, Inst Med Sci, Div Mol Therapy, Minato Ku, Tokyo 1088639, Japan

[4] Saitama Canc Ctr, Ina, Saitama 3620806, Japan

[5] RIKEN, Tsukuba Life Sci Ctr, Mol Genet Lab, Tsukuba, Ibaraki 3050074, Japan

[6] Inst Canc Res, Dept Cell Biol, Toshima Ku, Tokyo 1708455, Japan

[7] Tohoku Univ, Grad Sch Med, Dept Cell Biol, Sendai, Miyagi 9808575, Japan

来源：

GENES & DEVELOPMENT | 2003年 / 17卷 / 10期

关键词：

Tob; liver cancer; corepressor; cyclin D1 expression;

D O I：

10.1101/gad.1088003

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Tob is a member of antiproliferative family genes. Mice lacking tob are prone to spontaneous formation of tu-Mors. The occurrence rate of diethylnitrosamine-induced liver tumors is higher in tob(-/-) mice than in wildtype mice. tob(-/-)p53(-/-) mice show accelerated tumor formation in comparison with single null mice. Expression of cyclin D1 mRNA is increased in the absence of Tob and is reduced by Tob. Tob acts as a transcriptional corepressor and suppresses the cyclin D1 promoter activity through an interaction with histone deacetylase. Levels of tob mRNA are often decreased in human cancers, implicating tob in cancer development.

引用

页码：1201 / 1206

页数：6

共 35 条

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