Effects of lncRNA VPS9D1-AS1 on proliferation,apoptosis,and invasion of cervical cancer cells by regulating the miR-331-3p/SERP1 axis
Objective To investigate the effect and mechanism of lncRNA VPS9D1-AS1 on the malignant biological behavior of cervical cancer cells.Methods The expression of lncRNA VPS9D1-AS1 in cervical cancer cells and cervical can-cer tissues was analyzed.SiHa cells were separated into si-NC group,si-VPS9D1-AS1 group,si-VPS9D1-AS1+inhibitor NC group,and si-VPS9D1-AS1+miR-331-3p inhibitor group and control group.qRT-PCR was applied to detect transfection effi-ciency.A series of functional experiments such as colony formation assay,flow cytometry,Transwell assay and cervical cancer cell xenograft growth were applied to study the effect of lncRNA VPS9D1-AS 1 on cervical cancer.Luciferase reporter gene method and Western blotting method were applied to verify the targeting relationship between lncRNA VPS9D1-AS1 and miR-331-3p,and between miR-331-3p and SERP1.Results The expression of VPS9D1-AS1 was up-regulated in cervical cancer tissues and cells(P＜0.05).Compared with the si-NC group,the number of SiHa cell colony formation,the expression of PCNA and SERP1,the number of migration and invasion cells,the expression of MMP-2 and MMP-9 in the si-VPS9D1-AS1 group were decreased,and the apoptosis rate and the expression of Cleaved Caspase-3 were increased(P＜0.05).Downregulation of miR-331-3p was able to reverse the inhibitory effect of VPS9D1-AS1 knockdown on the malig-nant behavior of SiHa cells(P＜0.05).Dual luciferase reporter gene assay confirmed that miR-331-3p and lncRNA VPS9D1-AS1,miR-331-3p and SERP1 had a targeted regulatory relationship(P＜0.05).Nude mouse experiments showed that inhibiting the expression of VPS9D1-AS1 in vivo was able to obviously reduce the mass,volume,and SERP1 expression of transplanted tumors,and increase the expression of miR-331-3p(P＜0.05).Conclusion In cervical cancer tissues and cells,lncRNA VPS9D1-AS1 is up-regulated.Knockdown of VPS9D1-AS1 blocks the malignant progression of cervical cancer cells through regulating the miR-331-3p/SERP1 axis.
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