INK4a/ARF抑癌基因与食管癌的研究进展  

The progression of expression of INK4a-ARF tumor-suppress in esophagus carcinoma

作　　者：张双平[1] 王春利[2] 

机构地区：[1]山西医科大学研究生院,太原030001 [2]山西省肿瘤医院胸外二科

出　　处：《肿瘤研究与临床》2006年第2期137-139,共3页Cancer Research and Clinic

摘　　要：INK4a/ARF基因位于染色体9p21的CDKN2A位点,它编码两种蛋白p16INK4a和p14ARF,这两个蛋白均为细胞周期调控因子,分别通过p16INK4a/pRB途径和p14ARF/p53途径履行调控细胞周期的职责,对INK4a/ARF位点p16INK4a和p14ARF的结构功能以及与食管癌的关系进行综述。The INK4a-ARF locus is located on CDKN2A point in human chromosome 9p21 and is known to encode two functionally distinct tumor-suppressor genes p16INK4a （MTS1/CDKN2/INK4a/p16） and p14ARF, have been shown to play significant roles in cell-cycle regulation in cancer, p16 is encoded by the exon la-exon 2-exon 3 transcript and functions as a negative regulator of the cell cycle through its inhibition of cyclin-dependent kinases （CDKs） 4 and 6 and subsequent blockage of the cyclindependent phosphorylation of pRB . Thus, loss of p16 function leads to deregulation of pRB＂ s suppressive block of the Gl-to-S transition and cell proliferation. In contrast, p14ARF is encoded by the exon 1β-exon 2 transcript and acts upstream of p53. Biochemical evidence has demonstrated that p14ARF physically interacts with human double minute 2 （HDM2） gene product and consequently stabilizes p53, leading to G1 cell-cycle arrest. Overall, somatic mutation of the INK4a/ARF tumor suppressor locus, resulting in functionally deficient p16 and possibly p14ARF proteins, seems to be a prevalent event in the development of oesophagus carcinoma.

关 键 词：INK4A/ARF 抑癌基因 食管癌 

分 类 号：R735.1[医药卫生—肿瘤]