MiR-218 restrains proliferation of cervical cancer cells via targeted regulation of HMGB1/RAGE pathway.

Purpose To explore the role of micro ribonucleic acid (miR)-218 in cervical cancer (CC) and the regulatory mechanism between the high mobility group box 1 (HMGB1)/receptor for advanced glycation end-product (RAGE) pathway and miR-218. Methods The CC HeLa cells were first transfected with miR-218 mimic (miR-218 mimic group) or miR-218 negative control (NC group) using Lipofectamine 2000 transfection reagent, and those only added with Lipofectamine 2000 transfection reagent were taken as Control group. Then, quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the level of miR-218 in CC cell line. Besides, the migration and invasion abilities of the cells were measured via Transwell chamber assay, and the apoptosis was analyzed using a flow cytometer. Finally, the protein levels of HMGB1 and RAGE were determined via Western blotting. Results The expression of miR-218 declined in the CC HeLa cell line. After overexpression of miR-218, the proliferation ability of the CC cells was weakened, and the migration and invasion of CC cells were repressed. Moreover, miR-218 was observed to directly regulate the HMGB1/RAGE signaling pathway in a targeted manner to affect the proliferation and migration of CC cells. Conclusions MiR-218 inhibits the HMGB1/RAGE pathway to suppress the proliferation, migration and invasion of CC cells.