Four faces of cellular senescence

被引：1505
作者：
Rodier, Francis [2 ,3 ]
Campisi, Judith [1 ,4 ]
机构：
[1] Buck Inst Age Res, Novato, CA 94945 USA
[2] Univ Montreal, Inst Canc Montreal, Ctr Hosp, Res Ctr, Montreal, PQ H2L 4M1, Canada
[3] Univ Montreal, Dept Radiol Radio Oncol & Nucl Med, Montreal, PQ H3C 3J7, Canada
[4] Univ Calif Berkeley, Lawrence Berkeley Lab, Berkeley, CA 94720 USA
来源：
JOURNAL OF CELL BIOLOGY | 2011年 / 192卷 / 04期
基金：
美国国家卫生研究院;
关键词：
ONCOGENE-INDUCED SENESCENCE; DNA-DAMAGE RESPONSE; HISTONE DEACETYLASE INHIBITORS; HUMAN-DIPLOID FIBROBLASTS; LIFE-SPAN; IN-VIVO; REPLICATIVE SENESCENCE; HUMAN-CELLS; PREMATURE SENESCENCE; TRIGGERS SENESCENCE;
D O I：
10.1083/jcb.201009094
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Cellular senescence is an important mechanism for preventing the proliferation of potential cancer cells. Recently, however, it has become apparent that this process entails more than a simple cessation of cell growth. In addition to suppressing tumorigenesis, cellular senescence might also promote tissue repair and fuel inflammation associated with aging and cancer progression. Thus, cellular senescence might participate in four complex biological processes (tumor suppression, tumor promotion, aging, and tissue repair), some of which have apparently opposing effects. The challenge now is to understand the senescence response well enough to harness its benefits while suppressing its drawbacks.
引用
收藏
页码：547 / 556
页数：10
相关论文
共 131 条
[71]   Senescence-associated β-galactosidase is lysosomal β-galactosidase [J].
Lee, BY ;
Han, JA ;
Im, JS ;
Morrone, A ;
Johung, K ;
Goodwin, EC ;
Kleijer, WJ ;
DiMaio, D ;
Hwang, ES .
AGING CELL, 2006, 5 (02) :187-195
[72]   p53 Deficiency Leads to Compensatory Up-Regulation of p16INK4a [J].
Leong, Wai Fook ;
Chau, Jenny Fung Ling ;
Li, Baojie .
MOLECULAR CANCER RESEARCH, 2009, 7 (03) :354-360
[73]   Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling [J].
Lin, AW ;
Barradas, M ;
Stone, JC ;
van Aelst, L ;
Serrano, M ;
Lowe, SW .
GENES & DEVELOPMENT, 1998, 12 (19) :3008-3019
[74]   Senescent human fibroblasts increase the early growth of xenograft tumors via matrix metalloproteinase secretion [J].
Liu, Dan ;
Hornsby, Peter J. .
CANCER RESEARCH, 2007, 67 (07) :3117-3126
[75]   Augmented Wnt signaling in a mammalian model of accelerated aging [J].
Liu, Hongjun ;
Fergusson, Maria M. ;
Castilho, Rogerio M. ;
Liu, Jie ;
Cao, Liu ;
Chen, Jichun ;
Malide, Daniela ;
Rovira, Ilsa I. ;
Schimel, Daniel ;
Kuo, Calvin J. ;
Gutkind, J. Silvio ;
Hwang, Paul M. ;
Finkel, Toren .
SCIENCE, 2007, 317 (5839) :803-806
[76]   Expression of p16INK4a in peripheral blood T-cells is a biomarker of human aging [J].
Liu, Yan ;
Sanoff, Hanna K. ;
Cho, Hyunsoon ;
Burd, Christin E. ;
Torrice, Chad ;
Ibrahim, Joseph G. ;
Thomas, Nancy E. ;
Sharpless, Norman E. .
AGING CELL, 2009, 8 (04) :439-448
[77]   Modulation of mammalian life span by the short isoform of p53 [J].
Maier, B ;
Gluba, W ;
Bernier, B ;
Turner, T ;
Mohammad, K ;
Guise, T ;
Sutherland, A ;
Thorner, M ;
Scrable, H .
GENES & DEVELOPMENT, 2004, 18 (03) :306-319
[78]   The DNA damage signaling pathway is a critical mediator of oncogene-induced senescence [J].
Mallette, Frederick A. ;
Gaumont-Leclerc, Marie-France ;
Ferbeyre, Gerardo .
GENES & DEVELOPMENT, 2007, 21 (01) :43-48
[79]   Increased gene dosage of Ink4a/Arf results in cancer resistance and normal aging [J].
Matheu, A ;
Pantoja, C ;
Efeyan, A ;
Criado, LM ;
Martín-Caballero, J ;
Flores, JM ;
Klatt, P ;
Serrano, M .
GENES & DEVELOPMENT, 2004, 18 (22) :2736-2746
[80]   Delayed ageing through damage protection by the Arf/p53 pathway [J].
Matheu, Ander ;
Maraver, Antonio ;
Klatt, Peter ;
Flores, Ignacio ;
Garcia-Cao, Isabel ;
Borras, Consuelo ;
Flores, Juana M. ;
Vina, Jose ;
Blasco, Maria A. ;
Serrano, Manuel .
NATURE, 2007, 448 (7151) :375-U14
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