DNA damage-induce cell cycle checkpoints involve both p53-dependent and -independent pathways: role of telomere repeat binding factor 2

被引：12

作者：

Narayan, S ^{[1
]}

Jaiswal, AS

Multani, AS

Pathak, S

机构：

[1] Univ Florida, Coll Med, UF Shands Canc Ctr, Gainesville, FL 32610 USA

[2] Univ Texas, MD Anderson Canc Ctr, Dept Canc Biol, Houston, TX 77030 USA

[3] Univ Texas, MD Anderson Canc Ctr, Dept Lab Med, Houston, TX 77030 USA

来源：

BRITISH JOURNAL OF CANCER | 2001年 / 85卷 / 06期

关键词：

DNA damage; p53; telomere; TRF1; TRF2; cell cycle arrest; apoptosis;

D O I：

10.1054/bjoc.2001.2002

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Treatment of colon cancer cells with MNNG causes DNA damage with reduced telomeric signals in a p53-dependent manner, but increased cell cycle arrest in S-G(2)/M by both p53-dependent and independent mechanisms. Results also indicate that cellular levels of TRF2 may play a critical role in MNNG-induced cell cycle arrest and apoptosis of colon cancer cells. (C) 2001 Cancer Research Campaign.

引用

页码：898 / 901

页数：4

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