miR‑182‑5p contributes to radioresistance in nasopharyngeal carcinoma by regulating BNIP3 expression
- Wei He
- Hongyan Jin
- Qian Liu
- Quanxin Sun
Affiliations: Department of Oncology, Wuhan Puren Hospital, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, Hubei 430081, P.R. China, Department of Oncology, The Third People's Hospital of Hubei Province Affiliated to Jianghan University, Wuhan, Hubei 430033, P.R. China
- Published online on: December 10, 2020 https://doi.org/10.3892/mmr.2020.11769
Copyright: © He
et al. This is an open access article distributed under the
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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.