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MiR?182?5p contributes to radioresistance in nasopharyngeal carcinoma by regulating BNIP3 expression.

ABSTRACT: 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.

SUBMITTER: He W

PROVIDER: S-EPMC7751459 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature

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

He Wei W Jin Hongyan H Liu Qian Q Sun Quanxin Q

Molecular medicine reports 20201214 2

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 tw ...[more]

PMID: 33313953

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Project description:BackgroundAccumulating evidence indicates that dysregulation of miR-182-5p can serve as diagnostic and prognostic biomarkers for some cancers, whereas the role of miR-182-5p has not been explored in nasopharyngeal carcinoma (NPC). Our study aims to elucidate the biological function of miR-182-5p in NPC and the potential molecular mechanism involved.MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine miR-182-5p expression in NPC primary tissues and cell lines. Immunohistochemistry (IHC) for ZFP36L1 was conducted in NPC samples. Western blot was used to evaluate protein expression in cell lines. A series of functional assays were carried out to evaluate the roles of miR-182-5p and ZFP36L1 in tumor development and progression of NPC. Bioinformatics tools and luciferase reporter assays were utilized to identify the potential mechanisms of action. Moreover, rescue experiments were applied to explore whether ZFP36L1 mediated the effects of miR-182-5p in NPC.ResultsUp-regulation of miR-182-5p was significantly associated with tumor development and poor prognosis in patients with NPC. Functional study demonstrated that miR-182-5p overexpression enhanced, whereas suppression of miR-182-5p impeded NPC cell proliferation, migration, tumorigenesis and metastasis. Mechanistically, miR-182-5p interacted with ZFP36L1 at two sites in its 3' un-translated region (UTR) and repressed ZFP36L1 expression in NPC. Consistently, an inverse correlation was observed between the expression levels of miR-182-5p and ZFP36L1 using clinical NPC tissues, and down-regulation of ZFP36L1 in NPC predicts poor survival. Furthermore, overexpression of miR-182-5p in NPC was partly attributable to the transcriptional activation effect induced by hypoxia-inducible factor 1α (HIF-1α).ConclusionsOur data suggests that miR-182-5p facilitates cell proliferation and migration in NPC through its ability to down-regulate ZFP36L1 expression, and that the HIF-1α/miR-182-5p/ZFP36L1 axis may serve as a novel therapeutic target in the management of NPC.

Dataset Information

MiR?182?5p contributes to radioresistance in nasopharyngeal carcinoma by regulating BNIP3 expression.

Publications

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

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