Cell cycle arrest is not senescence

被引：166

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

页码：94 / 101

页数：8

共 68 条

[1] Chemokine signaling via the CXCR2 receptor reinforces senescence
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
[J]. CELL, 2008, 133 (06) : 1006 - 1018
[2] Tsc/mTORC1 signaling in oocytes governs the quiescence and activation of primordial follicles
Adhikari, Deepak
Zheng, Wenjing
Shen, Yan
Gorre, Nagaraju
Hamalainen, Tuula
Cooney, Austin J.
Huhtaniemi, Ilpo
Lan, Zi-Jian
Liu, Kui
[J]. HUMAN MOLECULAR GENETICS, 2010, 19 (03) : 397 - 410
[3] apoB and apobec1, two genes key to lipid metabolism, are transcriptionally regulated by p53
Ashur-Fabian, Osnat
Har-Zahav, Adi
Shaish, Aviv
Amram, Hila Wiener
Margalit, Ofer
Weizer-Stern, Orly
Dominissini, Dan
Harats, Dror
Amariglio, Ninette
Rechavi, Gideon
[J]. CELL CYCLE, 2010, 9 (18) : 3761 - 3770
[4] The gene expression program of prostate fibroblast senescence modulates neoplastic epithelial cell proliferation through paracrine mechanisms
Bavik, C
Coleman, I
Dean, JP
Knudsen, B
Plymate, S
Nelson, PS
[J]. CANCER RESEARCH, 2006, 66 (02) : 794 - 802
[5] When cells get stressed: an integrative view of cellular senescence
Ben-Porath, I
Weinberg, RA
[J]. 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
Bhaumik, Dipa
Scott, Gary K.
Schokrpur, Shiruyeh
Patil, Christopher K.
Orjalo, Arturo V.
Rodier, Francis
Lithgow, Gordon J.
Campisi, Judith
[J]. AGING-US, 2009, 1 (04): : 402 - 411
[7] Prevention of cancer by inhibiting aging
Blagosklonny, Mikhail V.
[J]. 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
Blagosklonny, Mikhail V.
[J]. REJUVENATION RESEARCH, 2008, 11 (04) : 801 - 808
[9] Aging and immortality - Quasi-programmed senescence and its pharmacologic inhibition
Blagosklonny, Mikhail V.
[J]. CELL CYCLE, 2006, 5 (18) : 2087 - 2102
[10] Cell senescence: Hypertrophic arrest beyond the restriction point
Blagosklonny, Mikhail V.
[J]. JOURNAL OF CELLULAR PHYSIOLOGY, 2006, 209 (03) : 592 - 597

← 1 2 3 4 5 6 7 →