miR‑802 inhibits the epithelial‑mesenchymal transition, migration and invasion of cervical cancer by regulating BTF3.

MicroRNA (miR)-802 has been discovered to be involved in the occurrence and development of numerous types of tumor; however, studies into the role of miR‑802 in cervical cancer are limited. Therefore, the present study aimed to investigate the regulatory effects of miR‑802 in cervical cancer cells. miR‑802 expression levels in cervical cancer tissue and cells were analyzed using reverse transcription‑quantitative (RT‑q)PCR, a dual‑reporter luciferase activity assay was used to identify the direct target gene of miR‑802, and RT‑qPCR and western blotting were performed to determine the relationship between miR‑802 and basic transcription factor 3 (BTF3). Cell viability, and migration and invasion were analyzed using Cell Counting Kit‑8 and Transwell assays, respectively. Finally, the expression levels of metastasis‑associated proteins, N‑cadherin and E‑cadherin, were determined using RT‑qPCR and western blotting. Decreased expression levels of miR‑802 were found in cervical cancer tissues and cells, and the overexpression of miR‑802 inhibited cell viability, migration and invasion. Moreover, miR‑802 was discovered to directly target BTF3 to inhibit its expression. Notably, the overexpression miR‑802 markedly reversed the promotive effect of BTF3 on cell viability, in addition to the migratory and invasive abilities of the cells. Simultaneously, the overexpression of miR‑802 significantly suppressed epithelial‑mesenchymal transition, and the expression levels of matrix metallopeptidase (MMP)2 and MMP9 in cells through regulating BTF3. In conclusion, the present study revealed that miR‑802 may suppress cervical cancer progression by decreasing BTF3 expression levels, indicating that it may represent a potential therapeutic target for the treatment and prognosis of patients with cervical cancer.