[MALAT1 inhibits proliferation and promotes apoptosis of SH-SY5Y cells induced by Aβ 25-35 via blocking PI3K/mTOR/GSK3β pathway].

Objective To investigate the effects of long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on cell cycle, proliferation and apoptosis in SH-SY5Y model cells of Alzheimer's disease (AD). Methods The AD model cells (SH-SY5Y human neuroblastoma cells) were constructed using Aβ _25-35 . The AD cells were randomly divided into five groups: control group, over-expressed empty victor (pCDH-EV) group, MALAT1 over-expression (pCDH-MALAT1) group, MALAT1 expression inhibition of empty victor (pSICOR-EV) group, and MALAT1 expression inhibition (pSICOR-shMALAT1) group. The cell proliferation activity of all the groups was detected by MTT assay. The cell cycle and apoptosis rate were detected by flow cytometry after 48 hours of transfection. Western blot analysis was used to test the expressions of BAX, Bcl-2, caspase-3 and PI3K/mTOR/GSK3β proteins in the five groups. Results The AD model cells, over-expression and inhibition expression of MALAT1 vectors were successfully constructed. Inhibited expression of MALAT1 significantly inhibited the proliferation of AD SH-SY5Y cells, promoted apoptosis and arrested cell cycle in G1 phase. Western blotting showed that the inhibited expression of MALAT1 up-regulated the expressions of BAX, caspase-3 and down-regulated the expression of Bcl-2. At the same time, the inhibited expression of MALAT1 significantly inhibited the expression of p-PI3K/p-mTOR/p-GSK3β. In addition, over-expression of MALAT1 reversed the above effects. Conclusion Konck-down of MALAT1 can inhibit the proliferation and promote the apoptosis of AD model cells via down-regulating the activity of PI3K/mTOR/GSK3β.