miR-182-5p contributes to radioresistance in nasopharyngeal carcinoma by regulating BNIP3 expression

Radioresistance is the primary roadblock limiting the success of treatment of nasopharyngeal carcinoma (NPC). microRNA (miRNA/miR)-182-5p has been reported to affect the sensitivity of cancer cells to irradiation; however, the role of miR-182-5p in NPC has not been assessed. The aim of the present study was to investigate the contribution of miR-182-5p to the radioresistance of NPC cells. The key mRNA and miRNA involved in NPC radioresistance were identified using bioinformatics analysis. The two cell lines used in the present study were 5-8F cells (radio-sensitive) and 5-8F-R cells (radioresistant). A dual-luciferase reporter assay system was used to validate the binding between BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) mRNA and miR-182-5p. Reverse transcription-quantitative PCR and western blotting were used to determine the RNA and protein expression levels. To obtain a deeper insight into the effects of the BNIP3/miR-182-5p axis on NPC radioresistance, Cell Counting Kit-8, wound healing, Transwell invasion and colony formation assays, as well as flow cytometry analysis were performed. The results showed that miR-182-5p and BNIP3 were up and downregulated, respectively, in 5-8F-R cells. BNIP3 was also confirmed to be the target of miR-182-5p, and miR-182-5p reversed the inhibitory effect of BNIP3 in 5-8F-R cells. The cellular experiments showed that upregulation of BNIP3 not only inhibited cell proliferation, viability, invasion and migration, but also promoted the apoptosis of 5-8F-R cells. However, the effects of BNIP3 were attenuated by the simultaneous upregulation of miR-182-5p. Thus, through downregulation of BNIP3, miR-182-5p contributed to radiation resistance of NPC cells.