Journal of Gastroenterology

, Volume 48, Issue 1, pp 125–131

IL-23R polymorphisms, HBV infection, and risk of hepatocellular carcinoma in a high-risk Chinese population

Authors

  • Yan Xu
    • Department of Epidemiology and Biostatistics, MOE Key Laboratory of Modern Toxicology, State Key Laboratory of Reproductive MedicineNanjing Medical University
  • Yao Liu
    • Department of Epidemiology and Biostatistics, MOE Key Laboratory of Modern Toxicology, State Key Laboratory of Reproductive MedicineNanjing Medical University
  • Shandong Pan
    • Department of Epidemiology and Biostatistics, MOE Key Laboratory of Modern Toxicology, State Key Laboratory of Reproductive MedicineNanjing Medical University
  • Li Liu
    • Department of Hepatobiliary SurgeryNantong Tumor Hospital
  • Jibin Liu
    • Department of Hepatobiliary SurgeryNantong Tumor Hospital
  • Xiangjun Zhai
    • Department of Infection DiseasesJiangsu Province Center for Disease Prevention and Control
  • Hongbing Shen
    • Department of Epidemiology and Biostatistics, MOE Key Laboratory of Modern Toxicology, State Key Laboratory of Reproductive MedicineNanjing Medical University
    • Section of Clinical Epidemiology, Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Cancer CenterNanjing Medical University
    • Department of Epidemiology and Biostatistics, MOE Key Laboratory of Modern Toxicology, State Key Laboratory of Reproductive MedicineNanjing Medical University
    • Section of Clinical Epidemiology, Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Cancer CenterNanjing Medical University
Original Article—Liver, Pancreas, and Biliary Tract

DOI: 10.1007/s00535-012-0620-1

Cite this article as:
Xu, Y., Liu, Y., Pan, S. et al. J Gastroenterol (2013) 48: 125. doi:10.1007/s00535-012-0620-1

Abstract

Background

The interleukin-23 receptor (IL-23R) plays an important role in the T-helper 17 cell-mediated inflammatory process and is also involved in tumor immune surveillance, which may be linked to carcinogenesis in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). In this study, we hypothesized that potentially functional genetic variants of the IL-23R gene may modify HCC risk.

Methods

We genotyped two single-nucleotide polymorphisms (SNPs) of IL-23R, rs6682925 and rs1884444, in a case–control study of 837 HCC cases, 899 HBV surface antigen (HBsAg)-positive controls, and 743 HBsAg-negative controls. A reporter gene assay was performed to evaluate the functional relevance of the rs6682925 SNP located at the promoter region of the IL-23R gene.

Results

We found that the two SNPs were associated with the risk of HCC when compared with both the HBsAg-positive and -negative controls. When compared with all controls, IL-23R rs6682925 and rs1884444 both increased the HCC risk in a recessive genetic model [rs6682925 CC vs. TT/TC: odds ratio (OR) 1.35, 95 % confidence interval (CI) 1.07–1.70; rs1884444 GG vs. TT/TG: OR 1.36, 95 % CI 1.05–1.77]. Furthermore, the variant C allele of rs6682925 in the promoter region of IL-23R was associated with increased reporter gene activity.

Conclusions

These findings indicate that genetic variants in IL-23R may contribute to HCC development.

Keywords

Interleukin-23 receptorPolymorphismHepatocellular carcinomaHBVReporter gene

Supplementary material

535_2012_620_MOESM1_ESM.doc (56 kb)
Supplementary Tables 1–3 (DOC 55 kb)

Copyright information

© Springer 2012