| Objective: By filtrate the involved molecule through bioinformatics,this study aimed to investigate the relationship between abnormal expression of EIF3 D and occurrence and development of ovarian cancer through detecting the protein in different kind of ovarian tissues.Meanwhile,in vitro experiment,this study observed the effect on proliferation and cell cycle by knocking down EIF3 D in ovarian cancer cells,in order to explore the relevant mechanism.Methods: Bioinformatics was used to filtrate the molecule different between ovarian cancer and ovarian normal tissues.Immunohistochemistry was used to detecting the expression of EIF3 D in benign ovarian cystadenoma,borderline cystadenoma,and ovarian epithelial cancer,analyzed by Kruskal–Wallis nonparametric 1-way analysis.EIF3 D was knocked down in ovarian cancer cell lines CAOV-3 and SKOV-3 through Lv-shRNA and verified by qPCR and Western-blot.MTT assay was performed to detect the proliferation ability and unicellular clone ability was tested using colony formation assay.Data was compared with t test.The change of cell cycle after EIF3 D knockdown was revealed by flow cytometry,while relevant altered protein was measured using Western-blot.Results: We have filtrated some molecular by bioinformatics such as EIF3 D and SFRP3,and verified them by qPCR.It is showed that EIF3 D was elevated gradually in malignant transformation process(P<0.05).Furthermore,the expression of EIF3 D was positively correlated to the FIGO stages(P < 0.05)but seems existed no correlations with the subtypes(P>0.05)in ovarian cancer.EIF3 D was obviously knockdown by Lv-shRNA in ovarian cancer cell lines CAOV-3 and SKOV-3,which induced inhibition on cell proliferation ability and clone ability(P<0.05).Flow cytometry revealed that cells were arrest at G2/M phase of cell cycle(P<0.05),and CDK1 was also found down-regulated after EIF3 D silencing.Conclusion: Overexpression of EIF3 D could promote the occurrence and development of ovarian cancer while EIF3 D knockdown may induce G2/M arrest. |
