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细胞衰老在衰老和癌症中的意义。

Significance of cellular senescence in aging and cancer.

机构信息

Department of Biological, Chemical and Physical Sciences, Roosevelt University, Chicago, IL 60605, USA.

出版信息

Cancer Res Treat. 2009 Dec;41(4):187-95. doi: 10.4143/crt.2009.41.4.187. Epub 2009 Dec 31.

Abstract

Cellular senescence is a mechanism that induces an irreversible growth arrest in all somatic cells. Senescent cells are metabolically active but lack the capacity to replicate. Evolutionary theories suggest that cellular senescence is related to the organismal decline occurring in aging organisms. Also, such theories describe senescence as an antagonistically pleiotropic process that can have beneficial or detrimental effect on the organism. Cellular senescence is believed to be involved in the cellular changes observed as aging progresses. Accumulation of senescent cells appears to occur widely as the organism ages. Furthermore, senescence is a key element of the tumor suppressor pathways. Therefore, it is part of the natural barrier against the uncontrolled proliferation observed in cellular development of malignancies in multicellular organisms. Activation of the senescence process guarantees a limited number of cellular replications. The genetic network led by p53 is responsible for activation of senescence in response to DNA damage and genomic instability that could lead to cancer. A better comprehension of the genetic networks that control the cell cycle and induce senescence is important to analyze the association of senescence to longevity and diseases related to aging. For these reasons, experimental research both in vitro and in vivo aims to develop anticancer therapies based on senescence activation. The last decade of research on role and function of senescence in aging and cancer are discussed in this paper.

摘要

细胞衰老(Cellular senescence)是一种诱导所有体细胞不可逆生长停滞的机制。衰老细胞代谢活跃,但缺乏复制能力。进化理论表明,细胞衰老与衰老生物体内发生的机体衰退有关。此外,这些理论将衰老描述为一种拮抗多效性过程,对生物体可能有有益或有害的影响。细胞衰老被认为与衰老过程中观察到的细胞变化有关。随着生物体的衰老,衰老细胞的积累似乎广泛发生。此外,衰老还是肿瘤抑制途径的关键要素。因此,它是多细胞生物中恶性肿瘤细胞不受控制增殖的天然屏障的一部分。衰老过程的激活保证了细胞复制的有限数量。p53 领导的遗传网络负责激活衰老,以应对可能导致癌症的 DNA 损伤和基因组不稳定性。更好地理解控制细胞周期并诱导衰老的遗传网络对于分析衰老与长寿和与衰老相关疾病的关联非常重要。出于这些原因,体外和体内的实验研究旨在基于衰老的激活来开发抗癌疗法。本文讨论了过去十年关于衰老和癌症中衰老作用和功能的研究。

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本文引用的文献

1
A theory of age-dependent mutation and senescence.
Genetics. 2008 Aug;179(4):2061-73. doi: 10.1534/genetics.108.088526. Epub 2008 Jul 27.
2
p16(INK4a) translation suppressed by miR-24.
PLoS One. 2008 Mar 26;3(3):e1864. doi: 10.1371/journal.pone.0001864.
3
The guardian's little helper: microRNAs in the p53 tumor suppressor network.
Cancer Res. 2007 Dec 1;67(23):11099-101. doi: 10.1158/0008-5472.CAN-07-2672.
4
DNA damage, cellular senescence and organismal ageing: causal or correlative?
Nucleic Acids Res. 2007;35(22):7417-28. doi: 10.1093/nar/gkm681. Epub 2007 Oct 2.
5
Mutation accumulation affects male virility in Drosophila selected for later reproduction.
Physiol Biochem Zool. 2007 Sep-Oct;80(5):461-72. doi: 10.1086/520127. Epub 2007 Jul 13.
6
Dynamic assembly of chromatin complexes during cellular senescence: implications for the growth arrest of human melanocytic nevi.
Aging Cell. 2007 Aug;6(4):577-91. doi: 10.1111/j.1474-9726.2007.00308.x. Epub 2007 Jun 18.
7
Absence of senescence-associated beta-galactosidase activity in human melanocytic nevi in vivo.
J Invest Dermatol. 2007 Oct;127(10):2469-71. doi: 10.1038/sj.jid.5700903. Epub 2007 May 24.
8
p53 mediates senescence-like arrest induced by chronic replicational stress.
Mol Cell Biol. 2007 Aug;27(15):5336-51. doi: 10.1128/MCB.01316-06. Epub 2007 May 21.
10
Dose-dependent oncogene-induced senescence in vivo and its evasion during mammary tumorigenesis.
Nat Cell Biol. 2007 May;9(5):493-505. doi: 10.1038/ncb1567. Epub 2007 Apr 22.

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