LINC00609 inhibits A549 cells progression through the regulation of miR-128-3p/RND3 axis

Background:Long-chain non-coding RNA(lncRNA)LINC00609 is a potential tumor suppressor,but the mechanism of action in non-small cell lung cancer(NSCLC)is yet to be understood.Objectives:The effects of LINC00609 on A549 cell proliferation,apoptosis,and cell cycle arrest were investigated.Methods:The LINC00609 levels in NSCLC and normal tissues were analyzed by bioinformatics.Expressions of LINC00609,miR-128-3p,and Rho family GTPase 3(RND3)in NSCLC cells(A549)were determined by qRT-PCR.Bioinformatics analysis predicted target genes and dual-luciferase reporter assays to ensure that LINC00609 targeted miR-128-3p and miR-128-3p targeted RND3.The proliferation of cells was determined using EDU and CCK-8.Flow cytometry was used to evaluate cell apoptosis rate and cell cycle.The western blotting assay identified proteins related to proliferation and apoptosis.Results:In NSCLC tissues,LINC00609 was expressed in low levels,while its high expression was associated with a higher survival rate.LINC00609 affected cell proliferation,apoptosis,cell cycle arrest,and expression of related proteins.Dual-luciferase reporter assay showed that LINC00609 binds specifically to miR-128-3p,and miR-128-3p binds to RND3.MiR-128-3p overexpression could neutralize the effects of LINC00609.A siRNA targeting RND3 could reverse the effect of the miR-128-3p inhibitor.Silencing RND3 resulted in a decrease in apoptosis rate and the number of cells in the S-phase and an increase in the number of cells in the G1-phase.Furthermore,phosphorylation levels of the AKT protein and mTOR protein,and Bcl2 expression,increased;however,the expression of RND3,Bax,and caspase3 decreased.Conclusions:LINC00609 regulated miR-128-3p/RND3 axis to modulate A549 cell proliferation,apoptosis,and cell cycle arrest.In the case of NSCLC,LINC00609 could be a potential target for therapy.