Greenspan Emily J, Jablonski Melissa A, Rajan Thiruchandurai V, Levine Joel, Belinsky Glenn S, Rosenberg Daniel W
Center for Molecular Medicine, UCHC School of Medicine, University of Connecticut Health Center, Farmington, CT 06030-3101, USA.
Carcinogenesis. 2006 Jul;27(7):1316-22. doi: 10.1093/carcin/bgi373. Epub 2006 Mar 2.
CpG island methylation (CIM) is an epigenetic mechanism for transcriptional silencing that occurs at various stages of colon tumorigenesis. CIM has been found in serrated adenomas and hyperplastic polyps. There is also evidence for hypermethylation in aberrant crypt foci (ACF) that are found in resected colons from cancer patients. Our study addresses promoter methylation of a tumor suppressor gene, RASSF1A, within the colonic epithelium of subjects undergoing screening colonoscopies in the absence of synchronous tumors. Patients included in this study were at elevated risk for colorectal cancer (CRC) based on family history, but without a previously occurring or synchronous colon carcinoma. ACF were identified using close-focus magnifying chromendoscopy and collected by biopsy in situ. We isolated ACF and adjacent normal colonic epithelium by laser capture microdissection (LCM) and studied methylation of the RASSF1A promoter region in ACF and in adjacent normal mucosa. Expression of RASSF1A was verified using quantitative real-time polymerase chain reaction (QRT-PCR). We found that 8.6% (3 out of 35) of ACF had K-ras mutations and 24% (6 out of 25) had RASSF1A hypermethylation. Our results demonstrate that RASSF1A hypermethylation and K-ras mutations are not mutually exclusive and are present in patients at elevated risk of CRC. Importantly, CIM of RASSF1A is an early epigenetic aberration, occurring in the absence of synchronous colon tumors and is not accompanied by field effects into the surrounding epithelium.
CpG岛甲基化(CIM)是一种转录沉默的表观遗传机制,发生在结肠肿瘤发生的各个阶段。CIM已在锯齿状腺瘤和增生性息肉中被发现。在癌症患者切除的结肠中发现的异常隐窝灶(ACF)中也有高甲基化的证据。我们的研究探讨了在没有同步肿瘤的情况下接受筛查结肠镜检查的受试者结肠上皮内肿瘤抑制基因RASSF1A的启动子甲基化情况。本研究纳入的患者基于家族史患结直肠癌(CRC)的风险较高,但之前没有发生过或同步发生结肠癌。使用近焦放大染色内镜识别ACF,并通过原位活检收集。我们通过激光捕获显微切割(LCM)分离ACF和相邻的正常结肠上皮,并研究ACF和相邻正常黏膜中RASSF1A启动子区域的甲基化情况。使用定量实时聚合酶链反应(QRT-PCR)验证RASSF1A的表达。我们发现8.6%(35个中的3个)的ACF有K-ras突变,24%(25个中的6个)有RASSF1A高甲基化。我们的结果表明,RASSF1A高甲基化和K-ras突变并非相互排斥,且存在于患CRC风险较高的患者中。重要的是,RASSF1A的CIM是一种早期表观遗传异常,发生在没有同步结肠肿瘤的情况下,且不伴有对周围上皮的场效应。