干扰素诱导蛋白16在结直肠癌中的表达及其与K-ras基因突变的相关性研究

Expression of interferon induced protein 16 in colorectal adenocarcinoma and its relation with K-ras gene

背景与目的:结直肠腺瘤-癌序列是目前公认的结直肠癌演变过程,该过程伴随一系列基因突变及蛋白的异常表达和积累。本研究旨在探讨结直肠癌发生、发展过程中干扰素诱导蛋白16(interferon induced 16,IFI16)表达及其与K-ras基因突变之间的相关性。方法:收集云南省第一人民医院病理科2008—2009年门诊及手术的结直肠正常黏膜组织、腺瘤和腺癌各发展阶段标本,应用免疫组化SP法检测IFI16表达情况;应用PCR-RFLP法对结直肠癌标本K-ras基因12密码子进行检测,并与IFI16进行相关性分析。结果:IFI16在结直肠腺癌与腺瘤、腺瘤与正常结直肠黏膜组织中蛋白表达差异均有统计学意义(49.2%vs 25%,P<0.05;25%vs 0%,P<0.05)。结直肠癌患者K-ras基因突变率为38.3%;K-ras基因变异与IFI16表达无相关性(55.2%vs 44.4%,P>0.05),但与IFI16异位表达差异有统计学意义(13.8%vs 72.2%,P<0.05),两者之间呈显著相关(r=0.635,P<0.01)。结论:IFI16参与了结直肠癌的发生、发展过程,K-ras基因突变与IFI16异位在结直肠癌的发生、发展过程中起重要作用。

Background and purpose：It is well known that CRC comes from the adenoma-carcinoma sequence.Along with the progression,mutations and aberrant protein expression constantly take place.In this study,we discussed the expression of IFI16 in its progression from normal colorectal organism to adenoma,and finally to adenocarcinoma.The relationship between K-ras gene mutation and IFI16 expression was also discussed.Methods： Immunochemistry was used to analyze the distribution and location of the IFI16 protein in normal colorectal,adenoma and adenocarcinoma organisms.PCR-RFLP was applied to study K-ras gene mutation.Results：The percentage of expression of the IFI16 protein differed significantly between adenocarcinoma to adenoma and between adenoma to normal colorectal organisms（49.2% vs 25%,P0.05;25 % vs 0%,P0.05,respectively）.The K-ras gene mutation rate was 38.3% in colorectal adenocarcinoma in Yunnan Province.There was no significant association between K-ras mutation and IFI16 protein expression（55.2% vs 44.4%,P0.01）,but the K-ras gene mutation is obviously associated with ectopic of the IFI16 protein from nucleus to cytoplasm（r=0.635,P0.01）.Conclusion：IFI16 plays an important role in the process from colorectal adenoma to adenocarcinoma.K-ras mutation is significantly associated with ectopic of the IFI16 protein and the ectopic may play an important role in development of colorectal adenoma to adenocarcinoma.