Purpose: To evaluate the therapeutic effect of heated (60 C) lipiodol via hepatic artery administration in VX2 rabbit liver cancer model. Materials and Methods: Thirty male New Zealand white rabbits were randomly divided into 3 groups with 10 rabbits for each group. VX2 carcinoma cells were surgically implanted into the left liver lobe. The tumors were allowed to grow for 2 weeks, and studies were performed until the diameter of tumors detected by ultrasonograph reaching 2 to 3 cm. Under the anaesthesia, transcatheter hepatic arterial embolization was performed and Doxorubicin-lipiodol (37ºC) (1 mL), lipiodol (60ºC) (1 mL) and control (physiological saline (37ºC) (1 mL)) were injected into hepatic artery of the 3 different groups. One week later, the volume of tumor was measured by ultrasonograph again. The serum of all rabbits was collected before injection and at 4 and 7 days after injection and the level of aspartate aminotransferase (AST) was checked. The survival period of 3 groups of rabbits after treatment was also recorded. During the last course of their disease, the rabbits were given some analgetics to relieve suffering. Results: The tumors' growth rate in lipiodol (60ºC) Background/Aims: Hepatocellular carcinoma (HCC) is one of the male-dominant cancers, and hepatitis C virus (HCV) is one of the causes of HCC. It was reported that androgen receptor (AR) is expressed in HCC and its surrounding tissues. Androgen signaling and AR may be involved in hepatocarcinogenesis. In this study, we investigated whether HCV interacts with androgen signaling in human hepatocytes. Methods: HCV protein expression vectors were co-transfected with AR-expression vectors and AR-responsive element-driven reporter vector into immortalized human hepatocytes (IHHs) and human hepatoma cell lines. Kinase inhibitors were used to examine the activation of the Akt, MAPK, and JAK/STAT3 pathways. Real-time PCR and Western blotting were performed. Cell culture grown HCV (HCVcc) were also used, and angiogenesis was evaluated by tubule formation assays in human coronary microvascular endothelial cells in the presence of 5 -androgen-1 -ol-3-one. Results: HCV enhances AR-responsive gene expression in the presence of androgen. HCV core protein has the strongest effects and induced AR activation associated with JAK/STAT signaling. HCVcc enhances VEGF mRNA expression and angiogenesis. Conclusions: HCV core protein is an enhancer in androgen signaling and can be expected to play an important role in HCV-related hepatocarcinogenesis. 