Long Non-coding RNA MEG3 Induces The Apoptosis Via Down-regulating Survivin Mediated By PI3K/Akt Signalings In Human Breast Cancer MCF-7 Cells

Objective: To explore the effect and mechanism of long non-coding RNA maternally expressed gene 3(Lnc RNA MEG3)on the apoptosis in human breast cancer MCF-7 cells.Method: The cell,which stably express Lnc RNA MEG3(refferred as MCF-7-G cells),was constructed in our lab.The MCF-7 cell,which only vector was transfected(refferred as MCF-7-C cells),was used as control.MCF-7-G cells,MCF-7-C cells and MCF-7 cells were cultured in DMEM medium supplement with 10% fetal bovine serum and 1% penicillin and streptomycin.The viability was analyzed by MTT.the apoptosis was observed by Hoechst33258 staining and flow cytometry.The expression of PI3 K,Akt and survivin,and phosphorylation of PI3 K and Akt was detected by wastern blot.All experiments above were executed in MCF-7-G cells treated with or without IGF-1(a PI3 K agonist)and YL294002(a PI3 K inhibitor).MCF-7 cell and MCF-7-C cells were employed as control.Results: Compared with MCF-7-C cells and MCF-7 cells,the expression of Lnc RNA MEG3 was significantly increased in MCF-7-G(p< 0.01),whereas the expression of Lnc RNA MEG3 has not substantial changes in MCF-7-C cells and MCF-7 cells(p> 0.05).The relative viability of MCF-7-G cells is 70.72% and much less than MCF-7-C cells and MCF-7 cells(p< 0.01).There is little between MCF-7-C cells and MCF-7 cells(p> 0.05).The apoptosis rate of MCF-7 cells?MCF-7-C cells and MCF-7-G cells was,respectively,5.32%?5.68% and 18.26%,MCF-7-G cells had a higher apoptosis rate,and less expression of Survivin and phosphorylation of both PI3 K and Akt than MCF-7-C cells and MCF-7 cells(p< 0.01).There was little for Survivin expression and phosphorylation of both PI3 K and Akt between MCF-7-C cells and MCF-7 cells(p> 0.05).The results above suggested that Lnc RNA MEG3 induced apoptosis in MCF-7 cells.MCF-7-G cells treated with IGF-1,a PI3 K agonist,had relatively higher viability(90.79% v 73.39%)and less apoptosis rate(13.65% v 19.21%),which indicated that MCF-7-G cells treated with IGF-1 had a stronger proliferation ability than MCF-7-G cells treated without IGF-1(p< 0.01).Furthermore,The treatment of IGF-1 resulted in the significant down-regulation of Survivin expression(p< 0.01)and the dramatic up-regulation of both PI3 K and Akt phosphorylation(p< 0.01)in MCF-7-G cells.MCF-7-G cells treated with YL294002,a PI3 K inhibitor,had relatively less viability(42.42% v 73.66%)and apoptosis rate(25.33% v 18.67%).Moreover,The treatment of IGF-1 was the cause of the significant down-regulation of survivin expression and phosphorylation of both PI3 K and Akt(p< 0.01)in MCF-7-G cells.The results above indicated that Lnc RNA MEG3 induced the apoptosis by inhibiting the Survivin expression and PI3K/Akt signalings in MCF-7-G cells.Conclusion: Lnc RNA MEG3 induced the apoptosis,which resulted from down-regulation of Survivin mediated by PI3K/Akt signalings in human breast cancer MCF-7 cells.