Transcript analysis of HCV tumor promoting effect

The hepatitis C virus (HCV) is one of the major risk factors for the development of hepatocellular carcinoma (HCC). Nevertheless, transgenic mice which express the whole HCV polyprotein (HCV-Tg) do not develop HCC. Whereas chronic HCV infection causes inflammation in patients, in HCV-Tg mice, the host immune reaction against viral proteins is lacking. We aimed to test the role of HCV proteins in HCC development on the background of chronic inflammation in vivo. We crossed the HCV-Tg mice which do not produce HCC with the Mdr2-knockout (Mdr2-KO) mice which develop inflammation-associated HCC, to generate Mdr2-KO/HCV-Tg mice. We studied the effect of the HCV transgene on tumor incidence, hepatocyte mitosis and apoptosis, and on gene expression in the liver of produced mice. The expression profile of HCV-Tg and not HCV-Tg mice on the MDR2-KO and control MDR2-heterozygous background had been tested. The non-tumorous liver tissue from 4 non-HCV-Tg Mdr2-heterozygous female mice, 5 HCV-Tg Mdr2-heterozygous female mice, 5 non-HCV-Tg Mdr2-KO female mice, 5 HCV-Tg Mdr2-KO female mice and 6 tumors developed by HCV-Tg MDR2-KO mice were submitted to the gene expression profiling. The non tumorous match of tumorous samples number 1-4 are HCV-Tg MDR2-KO samples 1-4, of tumorous sample 5,6 - HCV-Tg MDR2-KO sample 5.