国际肿瘤学杂志››2013,Vol. 40››Issue (3): 170-173.

• 综述 •上一篇下一篇

Evi-1基因的生物学作用及致肿瘤机制进展

丁向萍, 张锦华

  1. 730000甘肃省第二人民医院消化内科
  • 出版日期:2013-03-08发布日期:2013-02-25
  • 通讯作者:张锦华, Email: E-mail:zjh51272@163.com
  • 基金资助:

    甘肃卫生行业科研计划项目(编号:GSWST2010-23)

Oncogenic mechanism and biological effect of Evi-1 gene

DING Xiang-Ping, ZHANG Jin-Hua

  1. Department ofGastroenterology, Second People’s Hospital of GansuProvince , Lanzhou 730030, China
  • Online:2013-03-08Published:2013-02-25
  • Contact:ZHANG Jin-hua, E-mail: zjh51272@163.com E-mail:zjh51272@163.com

摘要:逆转录病毒结合位点-1(Evi-1)基因是首先在小鼠粒细胞白血病发现的逆转录病毒结合位点。鼠和人类的Evi-1基因91%的核酸序列和94%的氨基酸序列同源。在恶性血液系统病变及其他实体肿瘤中高表达,致肿瘤机制主要为通过抑制Smads而抑制转化生长因子-β(TGF-β)信号途径,调节细胞周期,促进血管生成,抑制JNK及激活AP-1等。

关键词:Evi-1基因,Smad3蛋白质,白血病,TGF-β信号传导,肿瘤

Abstract:Ecotropic viral integration site-1 (Evi-1) gene is first identified as a binding site for retrovirus in murine myeloid leukemia. The humanhomologue withthe murine in leukemia oncogene Evi-1 is about 91% of nuclear sequence and 94% of amino acid. Evi-1 gene is high expressed in myeloid malignancies and other tumors. The main tumorigenic mechanisms of Evi-1 gene include inhibiting TGF-β signal path by depressing Smad3, adjusting cell cycle, promoting angiogenesis, inhibiting JNK, activating AP-1, and so on.

Key words:Evi-1 gene,Smad3 protein,Leukemia,TGF-&beta,signal transduction,Neoplasms