The effects and mechanism of long non-coding RNA NEAT1 on cell proliferation and apoptosis in gastric carcinoma cells

Abstract

Objective To investigate the effect and mechanism of long non-coding RNA NEAT1 (lncRNA NEAT1) on proliferation and apoptosis of gastric carcinoma cells. Methods The expression level of lncRNA NEAT1 and normal gastric cell line GES-1 was measured by real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR). The AGS cell line was divided into three groups, si-NEAT1 group, si-Ctrl group and Blank group. The proliferation ability was measured by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay and clone formation assay. Apoptosis ability was tested by flow cytometry. The expression level of Phosphor-protein KinaseB (p-Akt), B cell lymphoma/leukemia-2 (bcl-2) and bcl-2 associated X protein (bax) protein was measured by Western blotting. Results The expression level of lncRNA NEAT1 in AGS, BSG823, Hs746T and MGC-803 cell line was significantly higher than that in GES-1 (P=0.000). CCK-8 demonstrated that the A450 nm of si-NEAT1 group was significantly lower than that in si-Ctrl and Blank group after culturing for 72 and 96 h (P=0.001). The number of clone formation cells in si-NEAT1 group was significantly lower than that in si-Ctrl group, (31.43±3.25)% vs. (67.27±5.81)%, P=0.000. The apoptosis rate of si-NEAT1 group was significantly higher than that in si-Ctrl group, (19.5±1.2)% vs. (3.7±0.3)%, P=0.000. The expression level of p-Akt and bcl-2 protein in si-NEAT1 group was significantly up-regulated, while bax down-regulated. Conclusion LncRNA NEAT1 was over-expressed in gastric carcinoma cell lines. Knockdown of lncRNA NEAT1 could inhibit the proliferation and induce apoptosis, possibly through down-regulation of p-Akt and bcl-2 protien, and up-regulation of bax. Key words: Long non-coding RNA NEAT1; Gastric carcinoma; Proliferation; Apoptosis