Polymorphism And Expression Of Antigen-presenting Molecule With Hepatitis B Virus-related Hepatocellular Carcinoma | 12196
ISSN: 2155-952X

Journal of Biotechnology & Biomaterials
Open Access

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Polymorphism and expression of antigen-presenting molecule with hepatitis B virus-related hepatocellular carcinoma

4th World Congress on Biotechnology

Bing Qiu, Wei Jiang, Fengxiang Wei, Xi Wang, Dongjie Liu, Ping Liu, Huijing Hu, Zhiyong Di and Jianying Zhang

Posters: J Biotechnol Biomater

DOI: 10.4172/2155-952X.S1.024

Background: Transporter associated with antigen processing (TAP) plays a central role in a cellular immune response against HBV. Objectives: The aim of this study was to evaluate the potential relationship between polymorphisms, expression of TAP and hepatitis B virus-related hepatocellular carcinoma. Methods: 189 HBV spontaneously recovered (SR) subjects, 196 liver cirrhosis (LC) and 195 hepatocellular carcinoma (HCC) individuals were included in this study. TAP1/2 was genotyped using a PCR-RFLP method. The expression of TAP1 in 38 HCC, 32 paratumor liver cirrhosis, and 28 normal liver tissues, was assessed by immunohistochemical assay using tissue microarray technology. Results: The frequency of TAP1-637-Gly was significantly higher in CHB and LC individuals than that in SR subjects (p = 0.024; p = 0.002), the significant difference of TAP2-651-Cys was observed between HCC cases and SR controls (p < 0.001), and TAP2- 687-Gln in CHB cases was more common than that in SR subjects (p = 0.021). The data also revealed that haplotype 687 Gln-651 Cys-637 Gly-333 Ile was strongly associated with CHB, LC and HCC (p < 0.001, < 0.05 and < 0.001, respectively). There was a significant difference of TAP1 positive rate in HCC and paratumor cirrhosis tissue compared with that in normal liver tissue (P < 0.0001, P < 0.01, respectively). Conclusions: TAP variants were likely to play a substantial role in the carcinogenesis process associated with persistent HBV infection, and the antigen presentation pathway restricted by MHC class I molecules was basically normal in HBV-related HCC.