From cirrhosis to hepatocellular carcinoma in HCV-infected patients: genes involved in tumor progression.

BACKGROUND

Hepatocellular carcinoma (HCC) is an aggressive tumor with poor prognosis. Understanding molecular changes in hepatocellular carcinoma should improve identification of risk factors in molecular subtypes and provide potential targets for early detection and therapy.

AIM

The present study aimed to analyze the molecular mechanism of the transition from hepatitis C virus (HCV) induced cirrhosis to HCV induced HCC using microarray analysis combined with bioinformatics techniques. METHODS, To accomplish this, we performed the differential coexpression analysis of hepatic gene expression in samples of HCV-cirrhotic patients with and without HCC. Total 465 genes were identified and some of them were used to construct a regulatory network.

RESULTS

Our analysis indicated that several differentially co-express genes might play crucial roles in HCC development, including NA3C2, AHR, MYC, FOXO1 and FOSB. Further analysis predicted these genes might be involved in HCC through pathways of "ribosome", "steroid biosynthesis", "spliceosome" and so on. Moreover, these genes may serve as potential therapeutic targets for the treatment of HCC.

CONCLUSIONS

In conclusion, our findings confirm the presence of multiple molecular alterations during HCV-infected HCC hepatocarcinogenesis and indicate the possibility for identifying prognostic factors associated with HCC progression.