Cellular senescence and DNA repair

被引：59

作者：

Lou, Zhenkun ^{[1
]}

Chen, Junjie ^{[1
]}

机构：

[1] Mayo Clin & Mayo Fdn, Div Oncol Res, Rochester, MN 55905 USA

来源：

EXPERIMENTAL CELL RESEARCH | 2006年 / 312卷 / 14期

关键词：

D O I：

10.1016/j.yexcr.2006.06.009

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Aging is a complex process that results in functional decline and mortality of the organisms. On the cellular lever, cellular senescence has been used as a model for aging. Therefore, understanding cellular senescence has important health implications. initial observations suggest that cellular senescence is the result of telomere shortening. Recent findings suggest that cellular senescence could be triggered by DNA damage. In fact, both telomere shortening and DNA-damage-induced cellular senescence share a common mechanism, the DNA damage response pathway. This review will discuss the link between DNA repair defects and cellular senescence. (c) 2006 Elsevier Inc. All rights reserved.

引用

页码：2641 / 2646

页数：6

共 52 条

[1] Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblasts [J].

Alcorta, DA ;

Xiong, Y ;

Phelps, D ;

Hannon, G ;

Beach, D ;

Barrett, JC .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (24) :13742-13747

[2] Disappearance of the telomere dysfunction-induced stress response in fully senescent cells [J].

Bakkenist, CJ ;

Drissi, R ;

Wu, J ;

Kastan, MB ;

Dome, JS .

CANCER RESEARCH, 2004, 64 (11) :3748-3752

[3] DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis [J].

Bartkova, J ;

Horejsi, Z ;

Koed, K ;

Krämer, A ;

Tort, F ;

Zieger, K ;

Guldberg, P ;

Sehested, M ;

Nesland, JM ;

Lukas, C ;

Orntoft, T ;

Lukas, J ;

Bartek, J .

NATURE, 2005, 434 (7035) :864-870

[4] ATM deficiency and oxidative stress: a new dimension of defective response to DNA damage [J].

Barzilai, A ;

Rotman, G ;

Shiloh, Y .

DNA REPAIR, 2002, 1 (01) :3-25

[5] Extension of life-span by introduction of telomerase into normal human cells [J].

Bodnar, AG ;

Ouellette, M ;

Frolkis, M ;

Holt, SE ;

Chiu, CP ;

Morin, GB ;

Harley, CB ;

Shay, JW ;

Lichtsteiner, S ;

Wright, WE .

SCIENCE, 1998, 279 (5349) :349-352

[6] Bypass of senescence after disruption of p21(CIP1/WAF1) gene in normal diploid human fibroblasts [J].

Brown, JP ;

Wei, WY ;

Sedivy, JM .

SCIENCE, 1997, 277 (5327) :831-834

[7] Senescent cells, tumor suppression, and organismal aging: Good citizens, bad neighbors [J].

Campisi, J .

CELL, 2005, 120 (04) :513-522

[8] Senescence aging, and malignant transformation mediated by p53 in mice lacking the Brcal full-length isoform [J].

Cao, L ;

Li, WM ;

Kim, S ;

Brodie, SG ;

Deng, CX .

GENES & DEVELOPMENT, 2003, 17 (02) :201-213

[9] Genomic instability in mice lacking histone H2AX [J].

Celeste, A ;

Petersen, S ;

Romanienko, PJ ;

Fernandez-Capetillo, O ;

Chen, HT ;

Sedelnikova, OA ;

Reina-San-Martin, B ;

Coppola, V ;

Meffre, E ;

Difilippantonio, MJ ;

Redon, C ;

Pilch, DR ;

Olaru, A ;

Eckhaus, M ;

Camerini-Otero, RD ;

Tessarollo, L ;

Livak, F ;

Manova, K ;

Bonner, WM ;

Nussenzweig, MC ;

Nussenzweig, A .

SCIENCE, 2002, 296 (5569) :922-927

[10] Human telomerase and its regulation [J].

Cong, YS ;

Wright, WE ;

Shay, JW .

MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS, 2002, 66 (03) :407-+

← 1 2 3 4 5 6 →