国际肿瘤学杂志

国际肿瘤学杂志 ›› 2013, Vol. 40 ›› Issue (8): 563-566.

• 综述 •    下一篇

FHIT基因与肿瘤

李娜, 贾秀红   

  1. 256603 滨州，滨州医学院附属医院儿科
  • 出版日期:2013-08-08 发布日期:2013-08-15
  • 通讯作者: 贾秀红，E-mail:jiaxiuhong001@163.com E-mail:jiaxiuhong001@163.com

FHIT gene and tumor

LI  Na, JIA  Xiu-Hong   

  1. Department of Pediatrics, the Affiliated Hospital of Binzhou Medical University, Binzhou 256603, China
  • Online:2013-08-08 Published:2013-08-15
  • Contact: Corresponding author: JIA Xiu-hong, E-mail:jiaxiuhong001@163.com E-mail:jiaxiuhong001@163.com

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1619

被引次数

15

摘要： 脆性组氨酸三联体(FHIT)基因是一种定位于人类染色体3p14.2上的抑癌基因,在多种器官中都有表达，其包含的脆性位点FRA3B，是基因组中最脆弱的部分。FHIT可促进细胞凋亡，抑制细胞增殖和细胞癌变。FHIT基因高度甲基化、基因缺失、FRA3B脆性位点的改变以及蛋白合成过程中的异常，可导致FHIT基因功能缺失，促进多种肿瘤的发生与发展。将野生型FHIT导入FHIT表达降低或者表达缺失的肿瘤细胞中可促进肿瘤细胞凋亡。FHIT基因与其他基因联合治疗可能为肿瘤的治疗提供新的方向。

关键词: 肿瘤, 细胞凋亡, 脆性组氨酸三联体

Abstract: The human fragile histidine triad (FHIT)gene is a tumor suppressor gene, which is located at chromosome region 3p14.2.The fragile site FRA3B of the FHIT gene is the most unstable site. FHIT can promote apoptosis, and inhibit cell proliferation and tumorigenesis. High methylation status, loss of the various sections of the FHIT gene, changes of the fragile site FRA3B and abnormalities of FHIT transcripts can result in gene afunction, and then promote the development and progression of various types of cancers. Transfecting wild-type FHIT into tumor cells with low or lacking endogenous FHIT expression can induce apoptosis. The combined treatment with other genes may provide a new insight for the treatment of tumors.

Key words: Neoplasms, Apoptosis, Fragile histidine triad