Survivin expression in esophageal cancer: correlation with p53 mutations and promoter polymorphism

被引:19
作者
Yang, Xiaoya [1 ]
Xiong, Gang [2 ]
Chen, Xuedan [1 ]
Xu, Xueqing [1 ]
Wang, Kai [1 ]
Fu, Yong [2 ]
Yang, Kang [2 ]
Bai, Yun [1 ]
机构
[1] Third Mil Med Univ, Dept Med Genet, Southwest Hosp, Chongqing, Peoples R China
[2] Third Mil Med Univ, Dept Thorac & Cardiac Surg, Southwest Hosp, Chongqing, Peoples R China
基金
中国国家自然科学基金;
关键词
esophageal cancer; P53; mutation; promoter polymorphism; survivin expression; SQUAMOUS-CELL CARCINOMA; ANTI-APOPTOSIS GENE; WILD-TYPE P53; DNA; OVEREXPRESSION; ACCUMULATION; PROGNOSIS; REGION; SITE;
D O I
10.1111/j.1442-2050.2008.00885.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Survivin is an inhibitor of apoptosis protein, which is selectively up-regulated in various cancers including esophageal cancer. The underlying mechanism of survivin overexpression in cancers is still unclear. We investigated resected tumor specimens from 100 esophageal cancer patients. Reverse transcription polymerase chain reaction was performed to evaluate survivin gene expression. Polymerase chain reaction-single strand conformation polymorphism was performed to investigate mutations of p53. We found that the survivin expression in tumors with mutant p53 is higher than that in tumors with wild type p53. Furthermore, the distribution of three polymorphisms in survivin promoter region in esophageal cancer patients was studied. The result indicated that the survivin expression was caused by a C allele in the survivin promoter polymorphism -625G/C in some degree. The methylation profile of survivin exon1 was also evaluated using bisulfite sequencing PCR. Our result indicated that survivin mRNA overexpression in cancer was not caused by its dysmethylation status. Therefore, our results suggested that the survivin expression depended on the p53 status and the C allele in the survivin promoter polymorphism -625G/C might increase the possibility of the survivin overexpression in esophageal cancer patients.
引用
收藏
页码:223 / 230
页数:8
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