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首页> 外文期刊>Experimental Gerontology >Molecular aspects of the relationship between cancer and aging: tumor suppressor activity during cellular senescence.
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Molecular aspects of the relationship between cancer and aging: tumor suppressor activity during cellular senescence.

机译：癌症与衰老之间关系的分子方面：细胞衰老过程中的抑癌活性。

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摘要

Normal cells cultured in vitro lose their proliferative potential after a finite number of doublings in a process termed replicative cellular senescence (Hayflick, 1965). The roles that growth inhibitory tumor suppressors play in the establishment and maintainence of cellular senescence have been reported in many different systems. The Rb and p53 tumor suppressors are examples of growth inhibitors that lose the ability to be regulated and are constantly activated during senescence. Other proteins that inhibit the initiation of DNA synthesis in early passage fibroblasts and that link the action of tumor suppressors with the cell cycle machinery, are also expressed at higher levels in senescent cells. For example, the increased expression of the cyclin-dependent kinase inhibitor p16 may contribute to arresting the growth of senescent cells. Identification and characterization of additional genes encoding growth inhibitors that are upregulated in senescent cells, such as the recently isolated p33ING1 protein, should provide a better understanding of the "aging program" that ceases to operate in the generation of immortal cancer cells.
机译：体外培养的正常细胞在被称为复制性细胞衰老的过程中经过有限的倍增后丧失了增殖能力（Hayflick，1965）。在许多不同的系统中已经报道了生长抑制性肿瘤抑制剂在细胞衰老的建立和维持中所起的作用。 Rb和p53肿瘤抑制剂是生长抑制剂的实例，这些抑制剂失去了被调节的能力，并在衰老过程中不断被激活。抑制早期传代成纤维细胞中DNA合成的起始并将肿瘤抑制因子的作用与细胞周期机制联系起来的其他蛋白质也以高水平在衰老细胞中表达。例如，细胞周期蛋白依赖性激酶抑制剂p16的表达增加可能有助于阻止衰老细胞的生长。鉴定和表征编码在衰老细胞中被上调的生长抑制剂的其他基因，例如最近分离的p33ING1蛋白，应该可以更好地理解永生癌细胞中不再起作用的“衰老程序”。

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