Open AccessHepatitis B virus mutations, expression quantitative trait loci for PTPN 12, and their interactions in hepatocellular carcinoma
Author(s) -
Song Ci,
Liu Yao,
Xu Lu,
Wen Juan,
Jiang Deke,
Chen Jianguo,
Zhai Xiangjun,
Hu Zhibin,
Liu Li,
Liu Jibin
Publication year - 2016
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.712
Subject(s) - hepatocellular carcinoma , hepatitis b virus , expression quantitative trait loci , biology , genotype , virology , single nucleotide polymorphism , virus , cancer research , gene , genetics
Previously we identified that HBV (Hepatitis B virus) sequence variation, which may interact with host human leukocyte antigen ( HLA ) genetic variation, could influence host risk of hepatocellular carcinoma ( HCC ). More HBV ‐host interactions need to be identified. Protein tyrosine phosphatase nonreceptor type 12 ( PTPN 12), serves as an antagonist to tyrosine kinase signaling, may play integral roles in immune response against HBV infection and the development of HCC . Rs11485985 was an expression quantitative trait loci ( eQTL ) for PTPN 12 by bioinformatics analyses. In this study, we genotyped the PTPN 12 eQTL and sequenced the HBV region Enh II / BCP / PC in a case–control cohort including 1507 HBV ‐related HCC cases and 1560 HBV persistent carriers as controls. The variant genotype GG of rs11489585 increased HCC risk compared to the HBV persistent carriers (adjusted OR = 2.03, 95% confidence interval [ CI s] = 1.30–3.18). We also detected borderline significant associations of PTPN 12 eQTL rs11489585 with HBV mutations ( P = 0.05 for G1799C). Taken together, PTPN 12 may influence HCC risk accompanied by HBV mutations.