Glioma is one of the most aggressive malignancies in the central nervous system and the prognosis of glioma patients remains poor. In this study, we investigated the function of microRNA-30e-3p (miR-30e-3p) in glioma development and its regulatory role in drug-resistance to temozolomide (TMZ). We found that miR-30e-3p was downregulated in glioma tissues and cell lines. Ectopic expression of miR-30e-3p inhibited the growth of glioma cells and arrested cell cycle at G0/G1 phase. Canopy FGF signaling regulator 2 (CNPY2) was predicted as a direct target of miR-30e-3p by bioinformatics analysis. Luciferase reporter assay confirmed the interaction between miR-30e-3p and CNPY2. We also demonstrated that miR-30e-3p suppressed glioma xenograft tumor development invivo and the inhibition was abolished by CNPY2 overexpression. In addition, we showed that overexpression of miR-30e-3p enhanced the sensitivity of glioma cell to TMZ treatment. Glioma cells with miR-30e-3p overexpression had decreased cell proliferation and enhanced cell apoptosis upon TMZ treatment. Moreover, we revealed that miR-30e-3p modulated TMZ sensitivity of glioma cells via negatively regulating CNPY2. Taken together, our findings demonstrate that miR-30e-3p plays a critical role in glioma development and drug sensitivity to TMZ treatment via negatively regulating CNPY2 expression. The study suggests that miR-30e-3p/CNPY2 could be developed as a novel target to improve the glioma therapy.Abbreviations: miR-30e-3p, microRNA-30e-3p; TMZ, temozolomide; CNPY2, canopy FGF signaling regulator 2; 3'-UTR, 3' untranslated region; NC, negative control.
Keywords: Glioma; microRNA-30e-3p; temozolomide.