[Corrigendum] miR­182­5p contributes to radioresistance in naso-pharyngeal carcinoma by regulating BNIP3 expression.

The authors have realized that, on p. 9 in the right­hand column, the second sentence featured in the final summary paragraph of the Discussion should have been deleted from the proofs prior to the publication of this article (the sentence that read as: 'This result indicated that downregulated BNIP3 expression may decrease the radioresistance of NPC cells.').Therefore, this sentence has been eliminated from the paper. The authors are grateful to the editor of Molecular Medicine Reports for allowing them to publish this Corrigendum, and all the named authors agree to its contents. The authors also apologize to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 23: 130, 2021; DOI: 10.3892/mmr.2020.11769].

miR­182­5p 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)­182­5p has been reported to affect the sensitivity of cancer cells to irradiation; however, the role of miR­182­5p in NPC has not been assessed. The aim of the present study was to investigate the contribution of miR­182­5p 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 5­8F cells (radio­sensitive) and 5­8F­R cells (radioresistant). A dual­luciferase reporter assay system was used to validate the binding between BCL2/adenovirus E1B 19 kDa protein­interacting protein 3 (BNIP3) mRNA and miR­182­5p. Reverse transcription­quantitative 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/miR­182­5p axis on NPC radioresistance, Cell Counting Kit­8, wound healing, Transwell invasion and colony formation assays, as well as flow cytometry analysis were performed. The results showed that miR­182­5p and BNIP3 were up and downregulated, respectively, in 5­8F­R cells. BNIP3 was also confirmed to be the target of miR­182­5p, and miR­182­5p reversed the inhibitory effect of BNIP3 in 5­8F­R cells. The cellular experiments showed that upregulation of BNIP3 not only inhibited cell proliferation, viability, invasion and migration, but also promoted the apoptosis of 5­8F­R cells. However, the effects of BNIP3 were attenuated by the simultaneous upregulation of miR­182­5p. Thus, through downregulation of BNIP3, miR­182­5p contributed to radiation resistance of NPC cells.