Statistical analysis indicated that the difference is significant (P<0.01).The animal experiments showed that tumors were formed in abdominal cavity in 70% mice of the FATE/BJ-HCC-2 gene-transfected group, but only in 10% mice of mock control group. Furthermore we also find tumor formation in livers of mice of the FATE/BJ-HCC-2 gene-transfected group with naked eyes and under light microscope. There was no tumor cell growth in liver of the mice of mock control group. Conclusion: FATE/BJ-HCC-2 could induce differential expression of a group of genes in tumor cells. It enhances invasion function of tumor cells. Tumor cells with FATE/BJ-HCC-2 expression are easier to form

tumors and tumor’s metastasis. This suggests that FATE/BJ-HCC-2 may be an important factor to promote metastasis of tumor cells. Disclosures: this website The following

people have nothing to disclose: Xiaoang Yang, Lili Ge, Junyan Piao, Yanhui Yin, Yu Zhang Background: Semaphorin7a (sema7a) is a membrane-anchored protein involved in neuronal and immune function regulating axonal growth, immune and inflammatory response. Recent evidences have confirmed an effect of sema7a on the regulation of bleomycin-induced pulmonary fibrosis. Our group have shown the involvement of sema7a in liver fibrogenesis, but no information are currently available on hepatocarcinogene-sis. Aims: to evaluate whether SEMA7A regulate HCC development. Methods: Liver injury was

induced in vivo by diethylnitrosamine (DEN) i.p. injection (25 mg/Kg) in 15 days old wild type and SEMA7A KO mice. Kupffer cells, hepatic stellate cells (HSCs) and hepatocytes GDC0068 were isolated with a nyco-denz-based gradient method from mice livers. Recombinant protein for SEMA7A was used for in vitro experiments in primary hepatocytes and human HepG2 cells. Results: In vivo, mice treated with DEN developed HCC formation after Gefitinib concentration 6 month from the treatment. The number of tumor nodules were significantly lower in SEMA7A KO mice than in WT mice, with an average of 8,2 macroscopic nodules in WT and 3,4 in the SEMA7A KO mice. Morevoer the average of the tumour size was 4.5 mm in WT vs 2 mm in SEMA7A KO. In vitro, we observed an increased expression of SEMA7A mRNA in hepatic stellate cells and in Kupffer cells isolated from fibrotic mouse livers, while a low expression was observed in hepatocytes. Hepatocytes do express one of the main receptor of sema7a: plexin C1, demonstrated by RT PCR. Moreover, primary hepatocytes from WT mice and human HepG2 cells, incubated with sema7a recombinant protein (1nM), show an increase in Ki67 mRNA, PCNA protein expression and a modification in the mRNA levels of carcinogenetic markers: 2.1 folds reduction and 4,1 fold increase respectively in PTEN and osteopontin mRNA expression vs untreated cells. Conclusions: SEMA7A is expressed in the liver and plays a crucial role in the development of HCC.