15087 Background: Anti-cancer bioactive peptide (ACBP) was extracted from the spleen of the goat suffered immune inducement by immunoreaction, supercentrifuge and ultra-filtration. Our previous studies have identified ACBP had significantly inhibited the growth of the human gastric cancer cell lines BGC-823 and MGC-803, the human rhinopharyngocele cell line CNE and the leukemic cell line. The in vivo experiments showed ACBP could dramatically repress the growth of tumor, and had few side-effects in the long-term toxic experiments. In clinical trials, ACBP could enhance the survival and life quality of the patients with advanced gastric cancer. In this study, we will explore the influence and mechanism of the effect of ACBP on cell cycle using human gastric cancer cell lines BGC-823 and MGC-803. Methods: Human gastric cancer cell lines BGC-823 and MGC-803 were cultured with different concentrations (10–25 ug/ml) of ACBP. The MTT method was employed to measure the growth inhibition rates of the cells with different concentrations of ACBP; the morphological changes were observed under the light microscope; the semi-quantitative RT-PCR was used to assay the changes of mRNA for p16,p21,p27,c-myc,cyclin D1,bax,bcl-2 gene. Results: Different concentrations of ACBP in the range of 10.0–25.0 μg/ml could inhibit the growth of BGC-823 and MGC-803 cell and such effect was both concentration and time dependent. 25.0 μg/ml ACBP had an inhibition rate (IR) of 84.4%, 72.3% and a median concentration (IC50) of 17.86 μg/ml, 13.16 ug/ml. After ACBP treatment, the cells showed typical apoptotic changes under the light microscope. On RT-PCR, the expressions of p16,p21,p27,bax mRNA in the two cell lines were markedly increased after ACBP treatment. On the contrary, the expression of c-myc,cyclin D1,bcl-2 mRNA in the two cell lines were obviously decreased after ACBP treatment. Conclusion: ACBP had markedly repressed the growth of BGC-823 and MGC-803 cell lines through inducing the cellular apoptosis. The possible mechanism is ACBP affects the cell cycle molecules expression including p16,p21,p27,cyclin D1 and regulate c-myc,bcl-2 and bax to induce apoptosis. No significant financial relationships to disclose.
LncRNA DSCR8 acts as a competitive endogenous RNA to regulate gastric cancer cell proliferation, invasion and cell cycle by mediating miR-137/Cdc42
