Farlier studies indicated that circular RNAs(circRNAs)were found in various cancer clls,and circFOXM1 was reported to act as an oncogane in non-small cell lung cancer(NSCLC).However,the function of circFOXM1 in NSCLC ...Farlier studies indicated that circular RNAs(circRNAs)were found in various cancer clls,and circFOXM1 was reported to act as an oncogane in non-small cell lung cancer(NSCLC).However,the function of circFOXM1 in NSCLC remains undear.The epression lewels of genes were measured using quantative real-time polymerase chain reactions(qRT-PCR).Cell prolferation and apoptosis were determined by 3-(4,5 dimethylthiazol-2-yl)-25 dipbenyletrazolium bromide solution(MTT)and flow cytometry assay.The rdative protein expression was assed by westen blot Moreower,transwell assays were employed to examine ell migration and invasion.The targeted relationship was confirmed by dual-luciferase reporter assay.The expression of circFOXMI was up-regulated in NSCIC tissues and cell lines.The depletion of circFOXM1 decreased the prolferation,migration,invasion,and induced cell apoptosis of NSCLC cells.MicroRNA-132-3p(MiR-1323p)was idenified as a target of dircFOXMl.The expression level of miR-132-3p was decrased in NSCLC tssues and cell lines and inversely corrdated with circFOXM1 expression.Furthermore,the efects of drdOXMl down regulation on NSCLC cell progression were abolished by mR-1323p inhibitor.Transmembrane protein 14A(TMEM14A)was verifed as a target gene of miR-132-3p.The efects of circFOXM1 depletion on NSCLC cell proliferation,apoptosis,migration,and invasion were reversed by TMEMI4A overexpression.Our study demonstrated that knodkdown of circFOXM1 suppressed NSCLC progression through rqgulating miR-132-3p/TMEMI4A axis,sugesting the drFOXM/miR-132-3p/TMEM14A axis may serve as the novd target for NSCLC diagnosis and therapy.展开更多
文摘Farlier studies indicated that circular RNAs(circRNAs)were found in various cancer clls,and circFOXM1 was reported to act as an oncogane in non-small cell lung cancer(NSCLC).However,the function of circFOXM1 in NSCLC remains undear.The epression lewels of genes were measured using quantative real-time polymerase chain reactions(qRT-PCR).Cell prolferation and apoptosis were determined by 3-(4,5 dimethylthiazol-2-yl)-25 dipbenyletrazolium bromide solution(MTT)and flow cytometry assay.The rdative protein expression was assed by westen blot Moreower,transwell assays were employed to examine ell migration and invasion.The targeted relationship was confirmed by dual-luciferase reporter assay.The expression of circFOXMI was up-regulated in NSCIC tissues and cell lines.The depletion of circFOXM1 decreased the prolferation,migration,invasion,and induced cell apoptosis of NSCLC cells.MicroRNA-132-3p(MiR-1323p)was idenified as a target of dircFOXMl.The expression level of miR-132-3p was decrased in NSCLC tssues and cell lines and inversely corrdated with circFOXM1 expression.Furthermore,the efects of drdOXMl down regulation on NSCLC cell progression were abolished by mR-1323p inhibitor.Transmembrane protein 14A(TMEM14A)was verifed as a target gene of miR-132-3p.The efects of circFOXM1 depletion on NSCLC cell proliferation,apoptosis,migration,and invasion were reversed by TMEMI4A overexpression.Our study demonstrated that knodkdown of circFOXM1 suppressed NSCLC progression through rqgulating miR-132-3p/TMEMI4A axis,sugesting the drFOXM/miR-132-3p/TMEM14A axis may serve as the novd target for NSCLC diagnosis and therapy.
