基础医学与临床 ›› 2017, Vol. 37 ›› Issue (7): 1051-1054.

• 短篇综述 • 上一篇    下一篇

坏死性凋亡与肿瘤

王莲子,李涛   

  1. 安徽医科大学第一附属医院
  • 收稿日期:2016-12-15 修回日期:2017-02-27 出版日期:2017-07-05 发布日期:2017-06-23
  • 通讯作者: 李涛 E-mail:limedical1974@126.com
  • 基金资助:
    国家自然基金

Necroptosis and tumor

Lian-zi LI Tao 2   

  • Received:2016-12-15 Revised:2017-02-27 Online:2017-07-05 Published:2017-06-23
  • Contact: LI Tao E-mail:limedical1974@126.com

摘要: 坏死性凋亡是不依赖于caspase激活的一种细胞程序性死亡方式,其激活主要依赖于坏死性小体的形成。坏死性凋亡的调控受到多种因素响,RIPK1既可启动坏死性凋亡,也可抑制坏死性凋亡;caspase-8是坏死性凋亡的重要负反馈调节蛋白;CHIP是新发现的坏死性凋亡调控蛋白。坏死性凋亡的触发为对经典凋亡途径抵抗的肿瘤提供了新的治疗策略。

关键词: 坏死性凋亡, RIPK, Caspase8, CHIP, 肿瘤

Abstract: Necroptosis, it is activated by the formation of necrosome, is a way of programmed cell death that independent of the activation of caspase. Necroptosis is regulated by many factors, for example, RIPK1 can initiate necroptosis, but also inhibit necroptosis; caspase-8 is the key negative regulation factor of necroptosis; CHIP is a new regulation protein of necroptosis. Triggering necroptosis is a promising strategy to overcome apoptosis resistance in cancer.

Key words: necroptosis, RIPK, Caspase8, CHIP, tumor

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