MicroRNA-101 Promotes the Proliferation, Migration, and Invasion of Uterine Cervix Cancer Cells by Targeting Cyclin-Dependent Kinase 8

Abstract

Uterine cervical cancer (UCC), or carcinoma of the uterine cervix, is a familiar malignancy in gynecology. The expression of multiple microRNAs is abnormal in UCC. Research has demonstrated that the level of microRNA-101 (miR-101) was decreased in UCC, but the mechanism by which miR-101 regulates UCC is still unclear. The TargetScan software predicted that one of the target genes of miR-101 was CDK8. This study aims to explore whether miR-101 affects the migration, invasion, and proliferation of UCC cells through CDK8. First, nanoparticle-assisted PCR was used to determine the levels of miR-101 and CDK8 in UCC tissues, normal adjacent tissues, and two UCC cell lines, C-33A and Siha. Compared to the normal tissues, the level of miR-101 was decreased in UCC tissues, while the level of CDK8 was increased. The dual-luciferase reporter experiments confirmed that miR-101 directly interacted with the binding site in CDK8 3’UTR to regulate luciferase activity. The UCC cells were transfected with the MIR101 mimic construct to overexpress miR-101. It was demonstrated that cell migration, invasion, and proliferation was reduced in C-33A cells overexpressing miR-101. In the cells co-transfected with CDK8 and MIR101, the overexpression of CDK8 reversed the effect of MIR101 overexpression on cell migration, invasion, and proliferation. Therefore, miR-101 can regulate the migration, invasion, and proliferation of UCC cells by targeting CDK8. Therefore, miR-101 has potential applications in the treatment of UCC.