The role of p53-target genes in human cancer

被引：149

作者：

Tokino, T ^{[1
]}

Nakamura, Y ^{[1
]}

机构：

[1] Univ Tokyo, Inst Med Sci, Ctr Human Genome, Mol Med Lab,Minato Ku, Tokyo 1088639, Japan

来源：

CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY | 2000年 / 33卷 / 01期

关键词：

p53; transcriptional activation; apoptosis; cell cycle; p53-target gene;

D O I：

10.1016/S1040-8428(99)00051-7

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The tumor suppressor gene p53 is mutated in a large proportion of human cancers. In some cellular conditions like DNA damage, the p53 gene is induced and its gene product is posttranscriptionally activated. p53 works as a transcriptional activator and induces the expression of its downstream target genes. This review will explain why expression of the normal p53 gene leads to tumor growth suppression. The p53 has several biological effects involving cell-cycle arrest, DNA replication and repair, proliferation, apoptosis, angiogenesis inhibition, and cellular stress response. These effects of the p53 result mainly from the activation of expression of a large number of p53-target genes. Here we have focused on the biological functions of the transcriptional targets of p53. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：1 / 6

页数：6

共 35 条

[1] Enhanced phosphorylation of p53 by ATN in response to DNA damage [J].

Banin, S ;

Moyal, L ;

Shieh, SY ;

Taya, Y ;

Anderson, CW ;

Chessa, L ;

Smorodinsky, NI ;

Prives, C ;

Reiss, Y ;

Shiloh, Y ;

Ziv, Y .

SCIENCE, 1998, 281 (5383) :1674-1677

[2] INDUCTION OF THE GROWTH INHIBITOR IGF-BINDING PROTEIN-3 BY P53 [J].

BUCKBINDER, L ;

TALBOTT, R ;

VELASCOMIGUEL, S ;

TAKENAKA, I ;

FAHA, B ;

SEIZINGER, BR ;

KLEY, N .

NATURE, 1995, 377 (6550) :646-649

[3] Activation of the ATM kinase by ionizing radiation and phosphorylation of p53 [J].

Canman, CE ;

Lim, DS ;

Cimprich, KA ;

Taya, Y ;

Tamai, K ;

Sakaguchi, K ;

Appella, E ;

Kastan, MB ;

Siliciano, JD .

SCIENCE, 1998, 281 (5383) :1677-1679

[4] CONTROL OF ANGIOGENESIS IN FIBROBLASTS BY P53 REGULATION OF THROMBOSPONDIN-1 [J].

DAMERON, KM ;

VOLPERT, OV ;

TAINSKY, MA ;

BOUCK, N .

SCIENCE, 1994, 265 (5178) :1582-1584

[5] DEFINITION OF A CONSENSUS BINDING-SITE FOR P53 [J].

ELDEIRY, WS ;

KERN, SE ;

PIETENPOL, JA ;

KINZLER, KW ;

VOGELSTEIN, B .

NATURE GENETICS, 1992, 1 (01) :45-49

[6] WAF1, A POTENTIAL MEDIATOR OF P53 TUMOR SUPPRESSION [J].

ELDEIRY, WS ;

TOKINO, T ;

VELCULESCU, VE ;

LEVY, DB ;

PARSONS, R ;

TRENT, JM ;

LIN, D ;

MERCER, WE ;

KINZLER, KW ;

VOGELSTEIN, B .

CELL, 1993, 75 (04) :817-825

[7]

Furuhata T, 1996, ONCOGENE, V13, P1965

[8] CSR, a scavenger receptor-like protein with a protective role against cellular damage caused by UV irradiation and oxidative stress [J].

Han, HJ ;

Tokino, T ;

Nakamura, Y .

HUMAN MOLECULAR GENETICS, 1998, 7 (06) :1039-1046

[9]

HARPER JW, 1993, CELL, V75, P805

[10] Mdm2 promotes the rapid degradation of p53 [J].

Haupt, Y ;

Maya, R ;

Kazaz, A ;

Oren, M .

NATURE, 1997, 387 (6630) :296-299

← 1 2 3 4 →