基础医学与临床 ›› 2008, Vol. 28 ›› Issue (5): 519-522.

• 短篇综述 • 上一篇    下一篇

细胞衰老:阻碍癌基因致癌的机制

孙倩 张宏冰   

  1. 中国协和医科大学基础医学院生理系 中国协和医科大学基础医学院生理系
  • 收稿日期:2007-07-17 修回日期:2007-09-04 出版日期:2008-05-25 发布日期:2008-05-25
  • 通讯作者: 张宏冰

Senescence is a defensive mechasim against oncogene-induced tumorigenesis

Qian SUN, Hong-bing ZHANG   

  1. Institute of Basic Medical Sciences,CAMS & PUMC Institute of Basic Medical Sciences,CAMS & PUMC
  • Received:2007-07-17 Revised:2007-09-04 Online:2008-05-25 Published:2008-05-25
  • Contact: Hong-bing ZHANG

摘要: 细胞衰老是生物体中普遍存在的一种永久性生长抑制现象,能够防止老化的或非正常细胞的进一步生长,对抗细胞的无限增殖能力而对机体起到保护作用。近年来,体内外研究表明癌基因诱导的细胞衰老能够抑制肿瘤的发生,但是一旦衰老机制缺陷,癌基因就会刺激细胞无限增殖而导致恶性肿瘤。已发现 ARF-p53 和 p16INK4a-RB 这两条途径的活化与细胞衰老的启动和调节过程密切相关。对细胞衰老的信号传导通路及其调节因子等方面的深入研究可能为肿瘤等重大疾病的预防和治疗提供帮助。

Abstract: Cellular senescence is a permanent cell cycle arrest that may prevent aged or abnormal cells from further expansion and is therefore a safeguard mechanism against unlimited cell proliferation. Recent studies demonstrated that oncogene-induced senescence could prevent neoplastic transformation in vitro and in vivo, and oncogene might cause tumors only in senescence deficient cells. Although the mechanism of the cellular senescence has not been completely illustrated, activation of p16INK4a-RB and ARF-p53 pathways has been implicated in this process. Further investigation of the signaling pathways leading to senescence may offer new avenues for tumor treatment.