Effect of lncRNA PSMA3-AS1 on the malignant biological behavior of cervical cancer cells by regulating the miR-224-3p/ARPP19 axis
Objective To explore the effect of long non-coding RNA human proteasome α subunit type 3 antisense RNA1(lncRNA PSMA3-AS1)on the malignant biological behavior of cervical cancer cells by regulating the mi-croRNA-224-3p(miR-224-3p)/cyclic adenosine phosphate protein 19(ARPP19)axis.Methods Cervical cancer HeLa cells were divided into si-PSMA3-AS1 group,si-NC group,si-PSMA3-AS1+miR-224-3p inhibitor group,si-PSMA3-AS1+inhibitor NC group and NC group.The relationship between miR-224-3p and lncRNA PSMA3-AS1 or ARPP19 was verified by dual luciferase reporter gene assay.The expression of lncRNA PSMA3-AS1 and miR-224-3p in HeLa,human cervical epithelial cell line HUCEC,and cervical cancer tissue were detected by qRT-PCR.The level of ARPP19 protein in cells and tissues were detected by Western blot.CCK8 method was applied to detect HeLa cell proliferation;flow cytometry was applied to detect HeLa cell apoptosis;the invasion and migration of HeLa cell were detected by Transwell.Immunocytochemical staining was used to detect the numbers of γδT and V81T positive cells.Results In cervical cancer tissue and HeLa cells,lncRNA PSMA3-AS1 and ARPP19 were highly expressed,while miR-224-3p was expressed at a low level.compared with NC group and si-NC group,the survival rate of HeLa cells,numbers of migration and invasive cells,level of lncRNA PSMA3-AS1 and ARPP19,the numbers of γδT and V81T positive cells in si-PSMA3-AS1 group were obviously decreased,and apoptosis rate of HeLa cells was obviously increased(P＜0.05).Inhibiting the expression of miR-224-3p weakened the effect of silencing lncRNA PSMA3-AS1 in inhibiting HeLa cell proliferation,migration,invasion,and promoting apoptosis.lncRNA PSMA3-AS1 negatively regulated the miR-224-3p/ARPP19 axis.Conclusion Suppression of lncRNA PSMA3-AS1 inhibits the malignant biological progression of HeLa cells,which may be achieved by regulating the miR-224-3p/ARPP19 axis.
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