Suppression of miR-93-5p inhibits high-risk HPV-positive cervical cancer progression via targeting of BTG3.

Abstract

This study explores the role of miR-93-5p in high-risk HPV-positive (HR-HPV) cervical cancer by targeting of BTG3. Cervical tissues were collected from 332 patients with conditions of chronic cervicitis (n = 42), low-grade cervical intraepithelial neoplasia (CIN I, n = 51), CIN II (n = 49), CIN III (n = 43), cervical cancer (n = 90), and normal cervical tissues (n = 57). HR-HPV DNA was detected by Hybrid Capture 2, and the expressions of miR-93-5p and BTG3 were determined by qRT-PCR and Western blot. The target relationship between miR-93-5p and BTG3 was verified by dual-luciferase reporter gene assay. HPV-positive cervical cancer cells (CaSki and HeLa) were divided into control, NC, inhibitor, BTG3, and mimic + BTG3 groups. CCK-8, Annexin V-APC/PI, and Transwell assays were applied to evaluate cell biological activities. MiR-93-5p was positively related but BTG3 was inversely related to HR-HPV infection. Additionally, miR-93-5p expression was negatively correlated with BTG3 expression in cervical cancer tissues infected with HR-HPV. HPV-positive cervical cancer cells showed higher miR-93-5p and lower BTG3 levels than negative cells. CaSki and HeLa cells in the inhibitor group showed increased BTG3 compared with the control group. After transfection with miR-93-5p inhibitor or BTG3 activation plasmid, proliferation and metastasis were inhibited, but apoptosis was promoted. The mimic + BTG3 group showed increased cell proliferation and metastasis but decreased cell apoptosis compared with the BTG3 group. Upregulated miR-93-5p was positively related but downregulated BTG3 was inversely related to HR-HPV infection, and inhibition of miR-93-5p may have blocked HPV-positive cervical cancer development by targeting of BTG3.