Biological functions of miR-183 on chemosensitivity of laryngeal cancer cells.

ABSTRACT

PURPOSE: The purpose of this study was to investigate the effect of miR-183 on the sensitivity of laryngeal cancer cells to 5-fluorouracil (5-Fu) and its mechanism, so as to provide certain references for the clinical prevention of drug resistance in laryngeal cancer cells. METHODS: Cell proliferation was determined via 5-ethynyl-2'-deoxyuridine (EdU) staining. Colony formation assay was applied to test the colony-formation ability in each group of cells. In addition, the expression levels of apoptosis-related proteins were measured through Western blotting. Wound-healing assay and Transwell assay were performed to examine the migratory and invasive abilities. Furthermore, the tumor-forming ability in vitro was detected by subcutaneous tumor formation assay. RESULTS: MiR-183 declined remarkably in 5-Fu-RES group compared with that in Control group. After overexpressing miR-183, the DNA replication and colony forming abilities of the resistant human primary laryngeal cancer cells were weakened notably. MiR-183 overexpression could obviously up-regulate Bax and inhibit Bcl-2 in the resistant human primary laryngeal cancer cells. Moreover, the overexpression of miR-183 was able to repress the migratory and invasive abilities of the resistant human primary laryngeal cancer cells. Further, overexpression of miR-183 restrained the in vitro tumor-forming ability of the resistant human primary laryngeal cancer cells markedly. Finally, it was revealed that TBX3 in the resistant human primary laryngeal cancer cells was suppressed distinctly, while that of PTEN was up-regulated evidently after overexpressing miR-183. CONCLUSIONS: The overexpression of miR-183 can inhibit the drug resistance of the human primary laryngeal cancer cells to 5-Fu, promote cancer cell apoptosis and inhibit their invasive and migratory abilities at the same time, whose mechanism may be associated with the targeted regulation of the TBX3/PTEN signaling pathway by miR-183.