长链非编码RNA MEG3对视网膜母细胞瘤增殖、迁移和侵袭能力的影响作用OA

Objective To investigate the effect of long non-coding RNA MEG3(LncRNA-MEG3)on the prolifera-tion,migration,and invasion abilities of retinoblastoma(RB).Methods The expression levels of MEG3,miR-145-5p,and the pro-apoptotic protein Bax mRNA were detected in RB cell lines(Weri-Rb1,Y79,HXO-Rb44)and human retinal pigment epithelial cells(hRPEC)using quantitative real-time polymerase chain reaction.The targeting relationship between miR-145-5p and MEG3 or Bax was validated through dual-luciferase reporter assays.Y79 cells were divided into the following groups:control group,oe-NC group,oe-MEG3 group,and corresponding rescue experiment groups in combination with miR-NC,miR-145-5p mimics,sh-NC,and sh-Bax.They were transfected with liposomes.Cell proliferation,migration,invasion,apopto-sis,and the expression of related proteins[rabbit anti-human nuclear antigen Ki67,matrix metalloproteinase-9(MMP-9),cleaved caspase-3,Bax,and B-cell lymphoma-2(Bcl-2)]were assessed using CCK-8 assay,Transwell assay,flow cytome-try,and Western blot,respectively.Results Compared to hRPEC,the expression of MEG3 and Bax mRNA was significant-ly downregulated,while the expression of miR-145-5p was significantly upregulated in all three RB cell lines(Weri-Rb1,Y79,and HXO-Rb44)(all P<0.05).Among them,Y79 showed the most pronounced changes and was therefore selected for subsequent experiments.The dual-luciferase assay confirmed that miR-145-5p could directly bind to the 3'-UTR regions of both MEG3 and Bax and inhibit their reporter gene activity.Overexpression of MEG3 significantly suppressed Y79 cell prolif-eration,migration,and invasion,promoted apoptosis,downregulated the protein expression of Ki67,MMP-9,and Bcl-2,and upregulated the protein expression of cleaved caspase-3 and Bax(all P<0.05).In rescue experiments,co-transfection with miR-145-5p mimics or knockdown of Bax partially reversed the above effects of MEG3 overexpression.Conclusion Overexpression of LncRNA-MEG3 can target and inhibit miR-145-5p,thereby upregulating the expression of Bax.Eventually,this suppresses the proliferation,migration,and invasion abilities of RB Y79 cells,and promotes cell apoptosis.