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细胞死亡与永生之间的分子联系(综述)

Molecular links between cellular mortality and immortality (review).

作者信息

Derventzi A, Rattan S I, Gonos E S

机构信息

National Hellenic Research Foundation, Institute of Biological Research and Biotechnology, Athens, Greece.

出版信息

Anticancer Res. 1996 Sep-Oct;16(5A):2901-10.

PMID:8917405
Abstract

Normal diploid cells cultivated in vitro exhibit limited division potential while undergoing ageing during serial passaging. In contrast, cells that have been genetically transformed appear to have lost the regulatory mechanisms of limited growth potential and may continue to divide indefinitely. While cellular mortality is characterised by a progressive cessation of cell growth manifested in cell culture by senescence, immortalisation is the escape from senescence as a result of multiple mechanisms involving the inactivation of tumour suppressor genes, the elevated expression of oncogenes, as well as other genetic and epigenetic changes. The mechanisms governing mortality and immortality are fundamentally linked. The physiological and biochemical features which characterise cellular mortality are examined, herein in the search for markers and timing mechanisms of mortality. The genetic elements involved in the control of mortality and immortality are also discussed, and the fundamental similarities between the molecular and genetic aspects which govern the determination of the phenotypes manifesting the two processes are underlined.

摘要

体外培养的正常二倍体细胞在连续传代过程中经历老化时,其分裂潜能有限。相比之下,经过基因转化的细胞似乎失去了有限生长潜能的调节机制,可能会无限期地继续分裂。细胞死亡的特征是细胞生长逐渐停止,在细胞培养中表现为衰老,而永生化则是由于多种机制导致的从衰老中逃脱,这些机制包括肿瘤抑制基因的失活、癌基因表达的升高以及其他遗传和表观遗传变化。控制细胞死亡和永生化的机制在根本上是相互关联的。本文研究了表征细胞死亡的生理和生化特征,以寻找死亡的标志物和时间机制。还讨论了参与控制细胞死亡和永生化的遗传因素,并强调了控制这两个过程所表现出的表型的分子和遗传方面的基本相似性。

相似文献

1
Molecular links between cellular mortality and immortality (review).细胞死亡与永生之间的分子联系(综述)
Anticancer Res. 1996 Sep-Oct;16(5A):2901-10.
2
The biology of replicative senescence.复制性衰老的生物学
Eur J Cancer. 1997 Apr;33(5):703-9. doi: 10.1016/S0959-8049(96)00058-5.
3
Over-expression of CDKIs p15INK4b, p16INK4a and p21CIP1/WAF1 genes mediate growth arrest in human osteosarcoma cell lines.细胞周期蛋白依赖性激酶抑制剂p15INK4b、p16INK4a和p21CIP1/WAF1基因的过表达介导人骨肉瘤细胞系的生长停滞。
In Vivo. 2001 Sep-Oct;15(5):443-6.
4
Multiple pathways to cellular senescence: role of telomerase repressors.细胞衰老的多种途径:端粒酶抑制因子的作用
Eur J Cancer. 1997 Apr;33(5):710-5. doi: 10.1016/S0959-8049(97)00090-7.
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[Immortality, cellular aging and death of cells. Role of protooncogenes, oncogenes and anti-oncogenes].[细胞永生、衰老与死亡。原癌基因、癌基因与抗癌基因的作用]
Postepy Biochem. 1993;39(4):212-20.
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Mass cultured human fibroblasts overexpressing hTERT encounter a growth crisis following an extended period of proliferation.大量培养的过表达hTERT的人成纤维细胞在长时间增殖后会遭遇生长危机。
Exp Cell Res. 2000 Sep 15;259(2):336-50. doi: 10.1006/excr.2000.4982.
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A stochastic model of cell replicative senescence based on telomere shortening, oxidative stress, and somatic mutations in nuclear and mitochondrial DNA.基于端粒缩短、氧化应激以及核DNA和线粒体DNA体细胞突变的细胞复制性衰老随机模型。
J Theor Biol. 2001 Dec 21;213(4):573-86. doi: 10.1006/jtbi.2001.2432.
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[Cell culture and its application proliferative life span and immortalization of cultured human cells].[细胞培养及其在培养的人类细胞增殖寿命和永生化中的应用]
Gan To Kagaku Ryoho. 1992 Jul;19(7):1091-8.
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Induced senescence in HeLa cervical carcinoma cells containing elevated telomerase activity and extended telomeres.在含有升高的端粒酶活性和延长的端粒的人乳头瘤病毒18型永生化宫颈癌细胞系(HeLa细胞)中诱导衰老
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Partial proteasome inhibition in human fibroblasts triggers accelerated M1 senescence or M2 crisis depending on p53 and Rb status.人类成纤维细胞中的部分蛋白酶体抑制会根据p53和Rb状态引发加速的M1衰老或M2危机。
Aging Cell. 2008 Oct;7(5):717-32. doi: 10.1111/j.1474-9726.2008.00425.x. Epub 2008 Aug 1.

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