Cell cycle arrest is not senescence

被引：167
作者：
Blagosklonny, Mikhail V. [1 ]
机构：
[1] Roswell Pk Canc Inst, Dept Cell Stress Biol, Buffalo, NY 14263 USA
来源：
AGING-US | 2011年 / 3卷 / 02期
关键词：
Cellular senescence; locked quiescence; growth stimulation; mTOR; rapamycin; gerossuppressants; GENE-EXPRESSION; GROWTH ARREST; STEM-CELLS; P53; CANCER; MTOR; QUIESCENCE; FIBROBLASTS; METABOLISM; SUPPRESSION;
D O I：
10.18632/aging.100281
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
DNA damaging agents and radiation, cytotoxins and anti-cancer drugs, telomere erosion and cytokines, culture shock and mitogenic stimuli, oncogenes and tumor suppressors can induce both cell cycle arrest and cellular senescence. Due to this semi-coincidence, senescence is confused with cell cycle arrest, or even more misleadingly, with growth inhibition. With such misconceptions, cellular senescence cannot be linked to organismal aging. Also, the relation between cancer and senescence is distorted. Here I discuss why the link between arrest and senescence is semi-coincidental and how senescence is related to aging and cancer.
引用
收藏
页码：94 / 101
页数：8
相关论文
共 68 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]   Tsc/mTORC1 signaling in oocytes governs the quiescence and activation of primordial follicles [J].
Adhikari, Deepak ;
Zheng, Wenjing ;
Shen, Yan ;
Gorre, Nagaraju ;
Hamalainen, Tuula ;
Cooney, Austin J. ;
Huhtaniemi, Ilpo ;
Lan, Zi-Jian ;
Liu, Kui .
HUMAN MOLECULAR GENETICS, 2010, 19 (03) :397-410
[3]   apoB and apobec1, two genes key to lipid metabolism, are transcriptionally regulated by p53 [J].
Ashur-Fabian, Osnat ;
Har-Zahav, Adi ;
Shaish, Aviv ;
Amram, Hila Wiener ;
Margalit, Ofer ;
Weizer-Stern, Orly ;
Dominissini, Dan ;
Harats, Dror ;
Amariglio, Ninette ;
Rechavi, Gideon .
CELL CYCLE, 2010, 9 (18) :3761-3770
[4]   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
[5]   When cells get stressed: an integrative view of cellular senescence [J].
Ben-Porath, I ;
Weinberg, RA .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 113 (01) :8-13
[6]   MicroRNAs miR-146a/b negatively modulate the senescence associated inflammatory mediators IL-6 and IL-8 [J].
Bhaumik, Dipa ;
Scott, Gary K. ;
Schokrpur, Shiruyeh ;
Patil, Christopher K. ;
Orjalo, Arturo V. ;
Rodier, Francis ;
Lithgow, Gordon J. ;
Campisi, Judith .
AGING-US, 2009, 1 (04) :402-411
[7]   Prevention of cancer by inhibiting aging [J].
Blagosklonny, Mikhail V. .
CANCER BIOLOGY & THERAPY, 2008, 7 (10) :1520-1524
[8]   Aging, stem cells, and mammalian target of rapamycin: A prospect of pharmacologic rejuvenation of aging stem cells [J].
Blagosklonny, Mikhail V. .
REJUVENATION RESEARCH, 2008, 11 (04) :801-808
[9]   Aging and immortality - Quasi-programmed senescence and its pharmacologic inhibition [J].
Blagosklonny, Mikhail V. .
CELL CYCLE, 2006, 5 (18) :2087-2102
[10]   Cell senescence: Hypertrophic arrest beyond the restriction point [J].
Blagosklonny, Mikhail V. .
JOURNAL OF CELLULAR PHYSIOLOGY, 2006, 209 (03) :592-597
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