Journal
DNA AND CELL BIOLOGY
Volume 36, Issue 8, Pages 693-708Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/dna.2017.3664
Keywords
DNA damage response; single-nucleotide polymorphism; mRNA expression; hepatitis C virus; hepatitis B virus; hepatocellular carcinoma
Funding
- National Science Center [UMO-2012/05/B/NZ5/01852]
- Medical University of Lodz, Poland, Research Programme [503/6-086-01/503-01]
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The molecular mechanism of hepatocellular carcinoma (HCC) is related to DNA damage caused by oxidative stress products induced by hepatitis B virus (HBV) or C (HCV) infection and exposure to environmental pollutants. Single-nucleotide polymorphisms (SNPs) of DNA damage response (DDR) genes may influence individual susceptibility to environmental risk factors and affect DNA repair efficacy, which, in turn, can influence the risk of HCC. The study evaluates a panel of 15 SNPs in 11 DDR genes (XRCC1, XRCC3, XPD, MUTYH, LIG1, LIG3, hOGG1, PARP1, NFIL1, FEN1, and APEX1) in 65 HCC patients, 50 HBV-and 50 HCVinfected non-cancerous patients, and 50 healthy controls. It also estimates the mRNA expression of nine DDR genes in cancerous and adjacent healthy liver tissues. Two of the investigated polymorphisms (rs1052133 and rs13181) were associated with HCC risk. For all investigated genes, the level of mRNA was significantly lower in HCC cancer tissue than in non-cancerous liver tissue. Seven of the investigated polymorphisms were statistically related to gene expression in cancer tissues. The disruption of DDR genes may be responsible for hepatocellular transformation in HCV-infected patients.
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