Background: Angiogenesis is improtant to hepatoma and decreasing of host immunity promotes the development of tumor. We want to study the effect and mechanism of apoptosis of mice implanted hepatoma cells induced by eukaryotic plasmid-mediated anti-angiogenesis and immmunopotentiation therapy. Methods: Mouse endostatin eukaryotic plasmid (pSecES) and mouse IL-12 (interleukin 12) eukaryotic plasmid (pmIL-12) were extracted and purified from E. coli. H22 hepatoma cells were inoculated into the leg muscle of mice, which was divided into four groups and injected with pSecES, pmIL-12, pSecES+pmIL-12 or pcDNA3.1 naked plasmid DNA respectively into implantation sites repeatedly. Tumor formation and its weight was evaluated. Tumor microvessel density, tumor infiltrating lymphocytes and apoptosis of tumor cells were assayed by CD31 staining, HE staining and TUNEL assay respectively. Results: Inoculated mice received pSecES, pmIL-12 injection formed tumor slowly with less microvessel density, more tumor infiltrating lymphocytes in the latter and more tumor apoptosis cells in both groups compared with pcDNA3.1 injection. There were much more tumor apoptosis cells in pSecES+pmIL-12 group (19.9±5.5 per 400× microscope field P<0.05) than any other single plasmid injection group (400× microscope field: pSecES 11.3±4.1, pmIL-12 14.6±3.2, pcDNA3.1 1.4±1.3). Conclusion: Tumor cells of implanted hepatoma in mice could be synergeticly induced to apoptosis by eukaryotic plasmid-mediated anti-angiogenesis and immunotherapy through inhibiting tumor angiogenesis and promoting tumor lymphocytes to infiltrate, by which mice implanted hepatoma was inhibited. (20, 40, 80, 160, 200 ng/mL) in a serum-free medium for 24 h. Cell proliferation was measured by Brdu incorporation analysis, untreated WB-F344 cells were taken as controls. After treatment with Wnt3a (160ng/mL) for 24 h, subcellular localization and protein expression of -catenin in WB-F344 cells treated and untreated with Wnt3a were examined by immunofluorescence staining and Western-blot analysis. CyclinD1 mRNA expression was determined by semi-quantitative reverse-transcript polymerase chain reaction (RT-PCR). mRNA levels of some phenotypic markers (AFP, CK-19, ALB) and two hepatic nuclear factors were measured by RT-PCR. Expressions of CK-19 and AFP protein were detected by Western-blot analysis. Results: Wnt3a promoted proliferation of WB-F344 cells. Stimulation of WB-F344 cells with recombinant Wnt3a resulted in accumulation of the transcriptional activator -catenin, together with its translocation into the nuclei, and up-regulated typical Wnt target gene cyclinD1. After 3 d of Wnt3a treatment in the absence of serum, WB-F344 cells retained their bipotential to express several specific phenotypic markers of hepatocytes and cholangiocytes, such as AFP, CK-19 following activation of the canonical Wnt signaling pathway. Conclusion: The canonical Wnt signaling pathway promotes proliferation and self-renewal of rat hepatic oval cells. The expression level of Bid and other pro-and anti-apoptotic proteins were detected by immunoblotting. Results: HBx/51 showed the most sensitive towards Dox treatment, and truncated Bid (tBid) was also only detected in this cell line. The level of Bax was also increased in HBx/51 cells. Conclusions: The carboxy-terminal of HBx may enhance the processing of Bid into tBid, which may contribute to increased sensitivity of the cell towards the Dox treatment.