The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression

被引:3423
作者
Coppe, Jean -Philippe [1 ]
Desprez, Pierre-Yves [2 ,3 ]
Krtolica, Ana [1 ]
Campisi, Judith [1 ,2 ]
机构
[1] Univ Calif Berkeley, Lawrence Berkeley Lab, Div Life Sci, Berkeley, CA 94720 USA
[2] Ruck Inst Age Res, Novato, CA 94945 USA
[3] Calif Pacific Med Ctr, Canc Res Inst, San Francisco, CA 94107 USA
关键词
aging; cancer; inflammation; proliferation; invasion; PLASMINOGEN-ACTIVATOR INHIBITOR; ONCOGENE-INDUCED SENESCENCE; PANCREATIC-CANCER CELLS; TISSUE GROWTH-FACTOR; CELLULAR SENESCENCE; REPLICATIVE SENESCENCE; HUMAN FIBROBLASTS; GENE-EXPRESSION; ENDOTHELIAL-CELLS; PREMATURE SENESCENCE;
D O I
10.1146/annurev-pathol-121808-102144
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Cellular senescence is a tumor-suppressive mechanism that permanently arrests cells at risk for malignant transformation. However, accumulating evidence shows that senescent cells can have deleterious effects on the tissue microenvironment. The most significant of these effects is the acquisition of a senescence-associated secretor phenotype (SASP) that turns senescent fibroblasts into proinflammatory cells that have the ability to promote tumor progression.
引用
收藏
页码:99 / 118
页数:20
相关论文
共 150 条
[1]   Chemokine signaling via the CXCR2 receptor reinforces senescence [J].
Acosta, Juan C. ;
O'Loghlen, Ana ;
Banito, Ana ;
Guijarro, Maria V. ;
Augert, Arnaud ;
Raguz, Selina ;
Fumagalli, Marzia ;
Da Costa, Marco ;
Brown, Celia ;
Popov, Nikolay ;
Takatsu, Yoshihiro ;
Melamed, Jonathan ;
di Fagagna, Fabrizio d'Adda ;
Bernard, David ;
Hernando, Eva ;
Gil, Jesus .
CELL, 2008, 133 (06) :1006-1018
[2]   Remodeling chromatin for senescence [J].
Adams, Peter D. .
AGING CELL, 2007, 6 (04) :425-427
[3]   Mitochondria, oxidants, and aging [J].
Balaban, RS ;
Nemoto, S ;
Finkel, T .
CELL, 2005, 120 (04) :483-495
[4]   Cancer and the chemokine network [J].
Balkwill, F .
NATURE REVIEWS CANCER, 2004, 4 (07) :540-550
[5]  
Barcellos-Hoff MH, 2000, CANCER RES, V60, P1254
[6]   The gene expression program of prostate fibroblast senescence modulates neoplastic epithelial cell proliferation through paracrine mechanisms [J].
Bavik, C ;
Coleman, I ;
Dean, JP ;
Knudsen, B ;
Plymate, S ;
Nelson, PS .
CANCER RESEARCH, 2006, 66 (02) :794-802
[7]   Reversal of human cellular senescence:: roles of the p53 and p16 pathways [J].
Beauséjour, CM ;
Krtolica, A ;
Galimi, F ;
Narita, M ;
Lowe, SW ;
Yaswen, P ;
Campisi, J .
EMBO JOURNAL, 2003, 22 (16) :4212-4222
[8]   CXCL12 overexpression and secretion by aging fibroblasts enhance human prostate epithelial proliferation in vitro [J].
Begley, L ;
Monteleon, C ;
Shah, RB ;
MacDonald, JW ;
Macoska, JA .
AGING CELL, 2005, 4 (06) :291-298
[9]   Inflammation-associated immune suppression in cancer: The roles played by cytokines, chemokines and additional mediators [J].
Ben-Baruch, A .
SEMINARS IN CANCER BIOLOGY, 2006, 16 (01) :38-52
[10]   The signals and pathways activating cellular senescence [J].
Ben-Porath, I ;
Weinberg, RA .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2005, 37 (05) :961-976