上海交通大学学报（医学版）

上海交通大学学报（医学版） ›› 2017, Vol. 37 ›› Issue (9): 1271-.doi: 10.3969/j.issn.1674-8115.2017.09.014?

• 综述 • 上一篇    下一篇

自噬在肿瘤上皮间质转化中的作用#br#

李泊宁，赖东梅   

  1. 上海交通大学  医学院附属国际和平妇幼保健院，上海 200030
  • 出版日期:2017-09-28 发布日期:2017-10-10
  • 通讯作者: 赖东梅，电子信箱：laidongmei@hotmail.com
  • 作者简介:李泊宁（1993—），女，硕士生；电子信箱：lbnkyrie@163.com
  • 基金资助:
    国家自然科学基金（81370678）；上海市教育委员会高峰高原学科建设计划（20152236)；上海市科学技术委员会项目（14411961500）

Effect of autophagy on epithelia-mesenchymal transition

LI Bo-ning, LAI Dong-mei   

  1. The International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China
  • Online:2017-09-28 Published:2017-10-10
  • Supported by:
     National Natural Science Foundation of China, 81370678; Shanghai Municipal Education Commission—Gaofeng Clinical Medicine Grant Support, 20152236；Project of Shanghai Municipal Science and Technology Commission, 14411961500

PDF (PC)

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摘要： 自噬是细胞清除老化元件和受损蛋白的过程，与肿瘤的产生和进展有密切联系。上皮间质转化（EMT）是上皮表型的细胞经 过一系列变化获得侵袭和迁移能力，产生间质特性的过程。自噬可能在低氧环境下清除缺氧诱导因子1（HIF-1）进而抑制EMT 相 关基因转录，抑制TGF-β/Smad 信号通路从而抑制EMT，通过选择性自噬适配器p62 对泛素化蛋白的作用调节EMT 转录因子抑制 EMT。对自噬与 EMT 关系的深入研究有助于找到肿瘤治疗的新靶点。

关键词:  自噬, 上皮间质转化, 缺氧诱导因子 1, p62

Abstract:

 Autophagy is a self-renewing cellular process by which defective proteins and aged organs are eliminated. It is noteworthy that autophagy correlates with the initiation and progression of cancer. During epithelial-mesenchymal transition (EMT), cells with epithelial phenotype gain mesenchymal characteristics, thus facilitate invasion and metastasis. Autophagy may suppress EMT by the following mechanisms, such as decreasing hypoxia inducible factor-1 (HIF-1) in hypoxia to downregulate transcription of EMT related genes, regulating TGF-β/Smad signaling pathway negatively, utilizing selective autophagy adaptor, p62, to modulate EMT transcription factors. Further studies of the association between autophagy and EMT may contribute to indentify new targets of cancer therapy.

Key words: autophagy, epithelial-mesenchymal transition, hypoxia-inducible factor 1, p62