Abstract
BackgroundIt is well known that chronic inflammation plays a pivotal role in the development of hepatitis B virus (HBV) related hepatocellular carcinoma (HCC). However, the causes behind aberrant expression of inflammation-related genes occurred in HCC remain unclear.MethodsWe performed array-based analyses to comprehensively investigate the contributions of DNA methylation and somatic copy number aberration (SCNA) to the aberrant expression of 1,027 inflammation-related genes in 30 HCCs and paired non-tumor tissues. The results were validated in public datasets and an additional sample set of 47 paired HCCs and non-tumor tissues.ResultsWe identified 252 differentially expressed, 125 aberrantly methylated and 287 copy number changed inflammation-related genes. Despite reasonable statistical power, among them, only 11 genes and 56 genes whose aberrant expression was associated with DNA methylation or SCNA, respectively. DNA methylation and SCNA together contributed to less than 30% aberrant expression of inflammation-related genes.ConclusionThese results suggest that molecular mechanisms other than DNA methylation and SCNA might play major role in the regulation of aberrant expression of inflammation-related gene in HBV-related HCCs.
Highlights
Hepatocellular carcinoma (HCC) is one of the most common cancers in the world
Among them, only 11 genes and 56 genes whose aberrant expression was associated with DNA methylation or somatic copy number aberration (SCNA), respectively
Expression, Methylation and Copy Number of Inflammation Genes in hepatocellular carcinoma (HCC). These results suggest that molecular mechanisms other than DNA methylation and SCNA might play major role in the regulation of aberrant expression of inflammation-related gene in hepatitis B virus (HBV)-related HCCs
Summary
The major risk factors for the development of HCC include infection with hepatitis B virus (HBV) or hepatitis C virus (HCV), aflatoxin exposure, and chronic alcohol abuse [1]. It has been reported that about 55% of HCC occurs in China, where the major etiological factor is chronic HBV infection [2]. Evidence has been accumulated to show that dysregulation of inflammation-related genes plays important roles in the development of HCCs [4, 5]. To the best of our knowledge, there are few, if any, comprehensive studies employing integrative analysis to simultaneously interrogate both genetic and epigenetic events contributing to the aberrant expression of genes in the inflammation pathway in HBV-related HCCs. It is well known that chronic inflammation plays a pivotal role in the development of hepatitis B virus (HBV) related hepatocellular carcinoma (HCC). The causes behind aberrant expression of inflammation-related genes occurred in HCC remain unclear
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