Liang G, Salem C E, Yu M C, Nguyen H D, Gonzales F A, Nguyen T T, Nichols P W, Jones P A
Department of Biochemistry and Molecular Biology, Urologic Cancer Research Laboratory, Los Angeles, California, 90033, USA.
Genomics. 1998 Nov 1;53(3):260-8. doi: 10.1006/geno.1998.5502.
Most investigations on the role of DNA methylation in cancer have focused on epigenetic changes associated with known tumor suppressor genes. This may have led to an underestimation of the number of CpG islands altered by DNA methylation, since it is possible that a subset of unknown genes relevant to cancer development may preferentially be affected by epigenetic rather than genetic means and would not be identified as familial deletions, mutations, or loss of heterozygosity. We used a recently developed screening procedure (methylation-sensitive arbitrarily primed-polymerase chain reaction to scan genomic DNA for CpG islands methylated in white blood cells (WBCs) and in tumor tissues. DNA methylation pattern analysis showed little interindividual differences in the WBCs and normal epithelium (adjacent to colon, bladder, and prostate cancer cells), but with some tissue-specific differences. Cancer cells showed marked methylation changes that varied considerably between different tumors, suggesting variable penetrance of the methylation phenotype in patients. Direct sequencing of 8 of 45 bands altered in these cancers showed that several of them were CpG islands, and 2 of these sequences were identified in GenBank. Surprisingly, three of the bands studied corresponded to transcribed regions of genes. Thus, hypermethylation of CpG islands in cancer cells is not confined to the promoters of growth regulatory genes but is also found in actively transcribed regions.
大多数关于DNA甲基化在癌症中作用的研究都集中在与已知肿瘤抑制基因相关的表观遗传变化上。这可能导致低估了因DNA甲基化而改变的CpG岛数量,因为有可能与癌症发展相关的一部分未知基因可能优先受到表观遗传而非遗传方式的影响,并且不会被识别为家族性缺失、突变或杂合性缺失。我们使用了一种最近开发的筛选程序(甲基化敏感的任意引物聚合酶链反应)来扫描基因组DNA,以寻找在白细胞(WBC)和肿瘤组织中甲基化的CpG岛。DNA甲基化模式分析显示,白细胞和正常上皮组织(与结肠癌、膀胱癌和前列腺癌细胞相邻)之间个体差异很小,但存在一些组织特异性差异。癌细胞显示出明显的甲基化变化,不同肿瘤之间差异很大,这表明患者中甲基化表型的外显率不同。对这些癌症中改变的45条带中的8条进行直接测序表明,其中几条是CpG岛,其中2条序列在GenBank中被识别。令人惊讶的是,所研究的三条带对应于基因的转录区域。因此,癌细胞中CpG岛的高甲基化不仅局限于生长调节基因的启动子,也存在于活跃转录区域。