MiR-520d-5p functions as a tumor-suppressor gene in cervical cancer through targeting PTK2

Abstract

ObjectivePTK2 has been reported to be involved in tumor progression, but its regulating mechanisms in cervical cancer (CC) remain to be elusive. MiRNA-520d-5p was demonstrated to regulate the expression of many genes and inhibit the development of human tumors. However, the functional mechanisms of miRNA-520d-5p in the regulation of cervical cancer are not fully understood. MethodsRT-qPCR was employed to detect the expression levels of miR-520d-5p and PTK2. Western blot was performed to detect the expression levels of proteins. Dual-luciferase reporter assay was utilized to investigate the associations between miR-520d-5p and PTK2. CCK-8 assay was carried out to measure cell proliferation. In addition, transwell assay and scratch assay were used for cell invasion and migration analysis. Flow cytometry was used to detect cell apoptosis of cervical cancer. ResultsThe expression levels of PTK2 were elevated in CC tissues and cells lines. It was found that PTK2 was a target gene of miR-520d-5p. The expression of miR-520d-5p was down-regulated in CC tissues, which was negatively correlated with the expression of PTK2. MiR-520d-5p inhibited the proliferation, migration, and invasion of CC cells. In addition, overexpression of miR-520d-5p resulted in apoptosis of CC cells. Finally, we demonstrated that miR-520d-5p inhibited the activation of PI3K/AKT signaling. ConclusionMiR-520d-5p suppressed the proliferation, invasion, and migration of CC cells via targeting PTK2.