Abstract
DNA methylation is an epigenetic mechanism in the pathogenesis of hepatocellular carcinoma (HCC). Here, we conducted a systematic meta-analysis to evaluate the contribution of DNA methylation to the risk of HCC. A total of 2109 publications were initially retrieved from PubMed, Web of Science, Cochrane Library, Embase, CNKI and Wanfang literature database. After a four-step filtration, we harvested 144 case-control articles in the meta-analysis. Our results revealed that 24 genes (carcinoma tissues vs adjacent tissues), 17 genes (carcinoma tissues vs normal tissues) and six genes (carcinoma serums vs normal serums) were significantly hypermethylated in HCC. Subgroup meta-analysis by geographical populations showed that six genes (carcinoma tissues vs adjacent tissues) and four genes (carcinoma tissues vs normal tissues) were significantly hypermethylated in HCC. Our meta-analysis identified the correlations between a number of aberrant methylated genes (p16, RASSF1A, GSTP1, p14, CDH1, APC, RUNX3, SOCS1, p15, MGMT, SFRP1, WIF1, PRDM2, DAPK1, RARβ, hMLH1, p73, DLC1, p53, SPINT2, OPCML and WT1) and HCC. Aberrant DNA methylation might become useful biomarkers for the prediction and diagnosis of HCC.
Highlights
Hepatocellular carcinoma (HCC) is one of the most frequent malignancies and the sixth leading cause of cancer-related deaths in the United States [1]
Our meta-analysis identified the correlations between a number of aberrant methylated genes (p16, Ras association domain family member1A (RASSF1A), Glutathione S-transferase pi 1 (GSTP1), p14, CDH1, Adenomatous polyposis coli (APC), Runtrelated transcription factor 3 (RUNX3), Suppressor of the cytokine signalling 1 (SOCS1), p15, O6-methylguanine-DNA methyltransferase (MGMT), Secreted frizzled-related protein 1 (SFRP1), WNT inhibitory factor 1 (WIF1), PR domain containing 2 (PRDM2), DAPK1, Retinoic acid receptor beta (RARβ), Human MutL homolog 1 (hMLH1), p73, Deleted in liver cancer 1 (DLC1), p53, Serine peptidase inhibitor (SPINT2), Opioid binding protein/cell adhesion molecule-like (OPCML) and Wilms tumor 1 (WT1)) and hepatocellular carcinoma (HCC)
The meta-analysis of p14, p15, p73, APC, SOCS1, MGMT, SFRP1, PRDM2, DAPK1, RARβ, IGF2 and hMLH1 genes methylation was performed between HCC tumor tissues vs adjacent tissues and HCC tumor tissues vs normal tissues
Summary
Hepatocellular carcinoma (HCC) is one of the most frequent malignancies and the sixth leading cause of cancer-related deaths in the United States [1]. Epigenetic modification is involved in HCC pathogenesis [3], and aberrant DNA methylation is the primary mediator of epigenetic changes in HCC [7]. Methylation of CpG islands in the gene promoters is recognized as a common epigenetic mechanism of transcriptional regulations [8, 9], and it has been shown to have a relation to the occurrence and development of several types of carcinomas [10,11,12,13,14]. Several studies have suggested that aberrant methylation of multiple tumor suppressor genes may contribute to the pathogenesis of HCC and epigenetic inactivation provides a prognostic value for determining the risk for the development of HCC [17, 18]
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