The Molecular Mechanism Of High Metastatic Human Ovarian Cancer Cell Line HO-8910Pm Proliferation,Migration And Apoptosis Induced By Paris Saponin I

Objective Paris Saponin I(PSI),which is an effective constituent of Rhizoma Paridis,contribute to anti-tumor,immuneregulation and cardiovascular protection effect cardiovascular.lt has been shown in recent studies that PSI could remarkably inhibit proliferation and migration on HO-8910PM, induce cell apoptosis. However,its exact further mechanism need further research.Methods According to the previous experimental results,HO-8910PM cells treated with PSI(1.5ug/ml) for48hours as the experimental group,and no drug treatment as the control group.Then, total RNA of HO-8910PM cells was extracted,amplified cRNA marked biotin,which allomixis with Illumina chip to scan,analyze by Illumina bead studio application software and DAVID database.Experiment was repeated twice.Screening several significant different expression genes,which related to tumor cells proliferation,apoptosis and migration,verified by RT-PCR.Results Gene chip suggested that there is a clear difference in123genes(diffscore less than-13or greater than13),in detail, expression of70genes were downregulated, expression of53genes were upregulated.It’s also shown that they correlate with apoptosis, proliferation, cycle,migration,invasion,angiogenesis and so on.Signaling pathway enrichment analysis showed that the classic MAP kinase pathway (ERK1/2,extracellular signal-regulated kinase),protein processing in endoplasmic reticulum and wnt signaling pathway had been activated.RT-PCR results showed that expression of WNT5A,PIK3C2B were downregulated and expression of JUN,PPP1R15A were upregulated, which consistented with the results of gene chip assay. However, contrary to the results of gene chip assay, expression of MYC CDH2,MAPKAPK3were downregulated. In addition, no statistically significant difference was observed in the expression of MYC gene..Conclusion PSI might upregulate JUN,PPP1R15A and downregulate WNT5A,PIK3C2B, CDH2,MAPKAPK3expression via MAP kinase pathway (ERK1/2,extracellular signal regulated kina-se),protein processing in endoplasmic reticulum and wnt signaling pathway,so as to inhibit HO-8910PM cell proliferation,migration and apoptosis induction.