Aging and cancer cell biology, 2009

被引:68
作者
Campisi, Judith [1 ,2 ]
Yaswen, Paul [2 ]
机构
[1] Buck Inst Age Res, Novato, CA 94945 USA
[2] Univ Calif Berkeley, Lawrence Berkeley Lab, Berkeley, CA 94720 USA
关键词
DNA damage response; FOXO transcription factors; inflammation; longevity; p53; PI3; kinases; sirtuins; telomeres; tumor suppression; GENOME MAINTENANCE; DEACETYLASE SIRT1; MICE; SENESCENCE; TELOMERES; TUMORIGENESIS; GROWTH; DAMAGE; LONGEVITY;
D O I
10.1111/j.1474-9726.2009.00475.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cancer is an age-related disease in organisms with renewable tissues. A malignant tumor arises in part from genomic damage, which can also drive age-related degeneration. However, cancer differs from many age-related degenerative diseases in that it entails gain-of-function changes that confer new (albeit aberrant) properties on cells, resulting in vigorous cell proliferation and survival. Nonetheless, interventions that delay age-related degeneration - for example, caloric restriction or dampened insulin/IGF-1 signaling - often also delay cancer. How then is the development of cancer linked to aging? The answer to this question is complex, as suggested by recent findings. This Hot Topic review discusses some of these findings, including how genomic damage might alter cellular properties without conferring mutations, and how some genes that regulate lifespan in organisms that lack renewable tissues might affect the development of cancer in mammals.
引用
收藏
页码:221 / 225
页数:5
相关论文
共 34 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]   A critical role for telomeres in suppressing and facilitating carcinogenesis [J].
Artandi, SE ;
DePinho, RA .
CURRENT OPINION IN GENETICS & DEVELOPMENT, 2000, 10 (01) :39-46
[3]   SirT1 Gain of Function Increases Energy Efficiency and Prevents Diabetes in Mice [J].
Banks, Alexander S. ;
Kon, Ning ;
Knight, Colette ;
Matsumoto, Michihiro ;
Gutierrez-Juarez, Roger ;
Rossetti, Luciano ;
Gu, Wei ;
Accili, Domenico .
CELL METABOLISM, 2008, 8 (04) :333-341
[4]   P53-dependent integration of telornere and growth factor deprivation signals [J].
Beliveau, Alain ;
Bassett, Ekaterina ;
Lo, Alvin T. ;
Garbe, James ;
Rubio, Miguel A. ;
Bissell, Mina J. ;
Campisi, Judith ;
Yaswen, Paul .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (11) :4431-4436
[5]   Mammalian telomeres and telomerase: why they matter for cancer and aging [J].
Blasco, MA .
EUROPEAN JOURNAL OF CELL BIOLOGY, 2003, 82 (09) :441-446
[6]   SIRT1 transgenic mice show phenotypes resembling calorie restriction [J].
Bordone, Laura ;
Cohen, Dena ;
Robinson, Ashley ;
Motta, Maria Carla ;
van Veen, Ed ;
Czopik, Agnieszka ;
Steele, Andrew D. ;
Crowe, Hayley ;
Marmor, Stephen ;
Luo, Jianyuan ;
Gu, Wei ;
Guarente, Leonard .
AGING CELL, 2007, 6 (06) :759-767
[7]   Cellular senescence: when bad things happen to good cells [J].
Campisi, Judith ;
di Fagagna, Fabrizio d'Adda .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2007, 8 (09) :729-740
[8]   Aging and cancer cell biology, 2007 [J].
Campisi, Judith .
AGING CELL, 2007, 6 (03) :261-263
[9]   Tumor suppressor HIC1 directly regulates SIRT1 to modulate p53-dependent DNA-damage responses [J].
Chen, WY ;
Wang, DH ;
Yen, RWC ;
Luo, JY ;
Gu, W ;
Baylin, SB .
CELL, 2005, 123 (03) :437-448
[10]   Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor [J].
Coppe, Jean-Philippe ;
Patil, Christopher K. ;
Rodier, Francis ;
Sun, Yu ;
Munoz, Denise P. ;
Goldstein, Joshua ;
Nelson, Peter S. ;
Desprez, Pierre-Yves ;
Campisi, Judith .
PLOS BIOLOGY, 2008, 6 (12) :2853-2868