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在理解衰老、复制性衰老、细胞更新与癌症之间关系方面的最新进展。

Recent progress in understanding the relationships among aging, replicative senescence, cell turnover and cancer.

作者信息

Warner Huber R

机构信息

Biology of Aging Program, National Institute on Aging, Bethesda, MD 20892, USA.

出版信息

In Vivo. 2002 Nov-Dec;16(6):393-6.

Abstract

The link between aging and cancer is more than just the increasing accumulation of mutations with time. Recent research provides evidence that senescent cells are not merely passive bystanders, but may promote cancer through degradation of the tissue microenvironment. Another critical factor in the relationship between aging and cancer is p53 function; its activity level is apparently finely tuned to suppress cancer while regulating both apoptosis and the replacement of damaged cells through stem cell proliferation. The deacetylase activity of the sir2 gene product plays a role in longevity regulation in invertebrates, and also regulates p53 function in mammals, implying yet another link between aging and cancer in mammals.

摘要

衰老与癌症之间的联系不仅仅是随着时间推移突变的不断积累。最近的研究表明,衰老细胞并非仅仅是被动的旁观者,而是可能通过组织微环境的退化促进癌症。衰老与癌症关系中的另一个关键因素是p53功能;其活性水平显然经过精细调节,既能抑制癌症,又能调节细胞凋亡以及通过干细胞增殖来替换受损细胞。sir2基因产物的去乙酰化酶活性在无脊椎动物的寿命调节中发挥作用,在哺乳动物中也调节p53功能,这意味着哺乳动物衰老与癌症之间存在另一种联系。

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