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

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 miR101. 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.

Automated summary

The decreased level of microRNA-101 in Uterine cervical cancer affects the migration, invasion, and proliferation of UCC cells by targeting CDK8. Potential applications in the treatment of UCC have been identified for miR-101 through its interaction with CDK8.