MiR520a-3p suppresses cell proliferation and metastasis by inhibiting the p65-NFκB pathway in glioblastoma.

Abstract

BackgroundmiR520a-3p has previously had its antitumorigenic role in various types of cancers revealed, and been predicted as a posttranscriptional regulator of the NFκB-subunit RELA gene. Thus, miR520a-3p could function in carcinogenesis through suppressing RELA.MethodsExpression of miR520a-3p and RELA mRNA was quantified in glioma and normal tissue, and the correlation between them was analyzed statistically. Also, receiver-operating characteristic (ROC)–curve analysis was performed. Effects of miR520a-3p on cell viability, colony formation, migration, and invasion wereexplored in vitro. Whether RELA was a direct target of miR520a-3p or not was analyzed. Finally, restoration of RELA on the effect of miR520a-3p overexpression on proliferation of glioblastoma cells was detected.ResultsData showed that miR520a-3p expression was aberrantly downregulated and associated with malignance in glioma tissue. Areas under ROC curves of miR520a-3p and RELA mRNA expression were 0.9483 and 0.5967, respectively. Also, miR520a-3p expression was statistically correlated with RELA mRNA level in grade III–IV glioma tissue. Transfection of miR520a-3p mimic significantly increased miR520a-3p expression, and resulted in significant suppression of proliferation, migration, and invasion of glioblastoma cells in vitro. miR520a-3p overexpression resulted in statistical downregulation of RELA, both in mRNA and protein levels. RELA was direct target of miR520a-3p. In addition, restoration of RELA significantly weakened the inhibitory effect of miR520a-3p overexpression on viability and EdU-labeled glioblastoma cells.ConclusionThese findings suggest that miR520a-3p should be helpful in auxiliary glioma diagnosis and can attenuate the proliferation and metastasis of glioblastoma through suppressing RELA, and thus could be an attractive therapeutic target to eliminate glioblastoma.