Influence of long non-coding RNA HOTAIR on proliferation and apoptosis of gastric cancer cells by targeted regulation of miR-206

Objective To investigate the influence of long non-coding RNA HOTAIR on proliferation and apoptosis of human gastric adenocarcinoma cells(AGS). Methods The expression level of HOTAIR in normal gastric epithelial cells(GES-1)and gastric cancer AGS cells as well as the expression levels of HOTAIR and microRNA-206(miR-206)in gastric cancer AGS cells transfected with si-RNA HOTAIR(si-HOTAIR)were detected by real-time fluorescence quantitative polymerase chain reaction(PCR). Bioinformatics was used to predict the binding site of HOTAIR and miR-206, and the targeting relationship between HOTAIR and miR-206 was verified by luciferase reporter assay. The cells were divided into control group, si-HOTAIR group, and si-HOTAIR plus miR-206 inhibitor group. CCK-8 and colony formation assay were used to detect the cell viability and proliferation ability in each group, apoptosis of cells was detected by flow cytometry, and immunoblot assay was used to detect the expression of related anti-apoptotic protein CDK9. Results Compared with normal GES-1 cells, the expression of HOTAIR in AGS cells was significantly higher(P<0.001), while expression of - miR-206 was significantly lower(P<0.01). The expression of HOTAIR in AGS cells transfected with si-HOTAIR significantly reduced(P<0.01), and the expression of miR-206 significantly increased(P<0.01). Experimental results showed that miR-206 mimics can significantly reduce the luciferase activity of the wild-type HOTAIR plasmid(P<0.01). Compared with the control group, the cellular proliferation ability of si-HOTAIR group significantly reduced, while the apoptosis ability significantly improved(P<0.001). Compared with the si-HOTAIR group, the cellular proliferation ability of si-HOTAIR plus miR-206 inhibitor group significantly increased, while apoptosis ability significantly reduced(P<0.01). Experimental results showed that si-HOTAIR can significantly reduce the expression of CDK9 protein, and miR-206 inhibitor can significantly reduce the inhibition function of si-HOTAIR on CDK9 expression. Conclusion HOTAIR can promote the proliferation of gastric cancer cells and inhibit the apoptosis of gastric cancer cells by targeted regulation of miR-206.