| Objective: To investigate the effect of miR-129-3p on the proliferation and apoptosis of Burkitt lymphoma cells by targeting and regulating the expression of Cyclin B/CDK1 and iASPP.Methods: CA46 and Raji cell lines were cultured by cell culture technique.The mRNA expression level of miR-129 in CA46 and Raji cells after was detected by qPCR after transfected with miR-129inhibitor/ inhibitor-NC and miR-129mimics/mimics-NC by liposome transfection.Cell flow assay was performed to detect the apoptosis and cell cycle changes of CA46 and Raji cells after the silencing of miR-129.MTT and BrdU assays were used to detect the effect of miR-129 on the proliferation of Burkitt lymphocytes.Western Blot was used to detect the expression levels of iASPP,p53/TAp63 and CDK1 after cell transfection.Luciferase reporter gene assay verified the targeted binding relationship between miR-129 and iASPP and CDK1.Results:1.miR-129 mimics up-regulated the expression of miR-129 and reduced the proliferation of CA46 and Raji cells while miR-129 inhibitor reduced the expression of miR-129,and reduced the apoptosis and apoptosis rate of CA46 and Raji cells,which was statistically significant compared with the negative control group(P < 0.05).2.miR-129 mimics down-regulated the expression level of iASPP in CA46 and Raji cells and up-regulated the levels of p53 and TAp63.miR-129 inhibitor induced adverse changes,with statistically significant differences compared with the negative control group(P <0.05).3.miR-129 inhibitor up-regulated the expression level of CDK1 in CA46 and Raji cells,miR-129 mimics down-regulated the expression level of CDK1,and increased the cell rate in G2/M phase,which was statistically significant compared with the negative control group(P < 0.05).4.Compared with the negative control group,there were statistically significant differences between the wild-type iASPP/CDK1 reporter gene vector and the miR-129 mimics/ miR-129 inhibitor co-transfection group(P < 0.05),and no statistically significant differences between the mutant co-transfection group(P > 0.05).5.miR-129 inhibitor increased the expression levels of nuclear proteins in CDK1 and iASPP,and down-regulated the expressions of p53 and TAp63.Knockdown of CDK1 reverses the down-regulation effect of miR-129,with statistically significant differences compared with the negative control group(P < 0.05).Conclusions:1.miR-129 regulates the proliferation and apoptosis of tumor cells as a tumor suppressor in Burkitt lymphoma.2.miR-129 regulates the proliferation and apoptosis of Burkit lymphoma by affecting the expression levels of p53 and TAp63 through iASPP.3.miR-129 regulates the proliferation and apoptosis of Burkitt lymphoma by blocking the cell cycle progression of Burkitt lymphoma with CDK1.4.iASPP and CDK1 are potential targets of miR-129 in Burkitt lymphoma cells.5.miR-129 synergistically regulates the expression of iASPP,p53 and TAp63 in Burkitt lymphoma cells in conjunction with CDK1. |