Abstract: Objective To investigate the mechanism of nucleus accumbens-1（Nac1 or NAC-1）protein on the proliferation of ovarian cancer cell line HO8910. Methods Specific NAC-1 siRNAs and one negative siRNA were individually transfected into HO8910 cells for 48 h . Levels of NAC-1, β-catenin, LRP6, cyclinD1, and survivin mRNA and protein were analyzed by real-time fluorescence quantitative PCR (qRT-PCR) and Western blotting, respectively. The cell proliferation was determined by MTT assay and plate clone formation assay. The distribution of cell cycle was assessed by flow cytometry. Results After NAC-1 siRNA treatment for 48 h, not only the NAC-1 gene was silenced in HO8910 cells, the cell growth was inhibited, and cell cycle arrested in G1 phase, but also the activity of Wnt/β-catenin signaling decreased significantly, which levels of β-catenin, cyclinD1, and survivin proteins, cyclinD1 and survivin mRNA all decreased, as compared with the control groups, the difference was statistically significant. However, NAC-1 gene silencing in ovarian carcinoma cells HO8910 did not affect levels of p-LRP6 protein, LRP6 mRNA and β -catenin mRNA, as compared with the control groups, the difference was not statistically significant. Conclusion NAC-1 enhance the activity of WNT signaling pathway through the regulation of β -catenin protein level, promote ovarian cancer HO8910 cell proliferation.

Key words: Nucleus accumbens-1, small interfering RNA, ovarian cancer, Cell proliferation, Cell cycle, Wnt/β-catenin signaling