Objective To investigate the effect of long non-coding RNA(lncRNA)GNAS-AS1 knockdown on the proliferation,invasion,migration,and cisplatin sensitivity of the gastric cancer cell line AGS.Methods Expression levels of GNAS-AS1 in gastric cancer cells were detected by quantitative reverse-transcription polymerase chain reaction(qRT-PCR).After transfection of GNAS-AS1 siRNA in AGS cells and induced with cisplatin,cell proliferation,cloning ability,and apoptosis were examined by cell counting kit-8(CCK-8)assay,colony formation assay and flow cytometry,respectively.Cell migration and invasion were detected by Transwell assay.Protein levels of cleaved caspase-3,matrix metalloproteinase-2(MMP-2)and MMP-9 were detected by Western blot.The target relationship between GNAS-AS1 and miR-362 was verified by Starbase prediction and dual-luciferase reporter assay.After co-transfection of GNAS-AS1 siRNA and miR-362 inhibitor,cell behaviors were similarly examined.Results GNAS-AS1 was upregulated in gastric cancer cells.Transfection of GNAS-AS1 siRNA in cisplatin-induced AGS cells inhibited the proliferation,cloning,migration,and invasion,and induced apoptosis.Knockdown of GNAS-AS1 targeted and upregulated miR-362.Transfection of miR-362 inhibitor reversed the role of GNAS-AS1 knockdown on the proliferation,cloning,apoptosis,migration and invasion of AGS cells.Conclusion Knockdown of lncRNA GNAS--S1 regulates the expression of miR-362,thereby reducing the proliferation,invasion and migration abilities of AGS and increasing cisplatin sensitivity.
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