Peroxiredoxin 3 (PRDX3) is an abundant and effective
enzyme, which
aids in the removal of H2O2 in the mitochondria, thereby inhibiting cell autophagy. PRDX3 is a target
protein of
microRNA (
miRNA/miR)-383, the overexpression of which has been found to inhibit the growth of
glioma cells. We hypothesized that miR-383 serves an antitumor role by inhibiting oxidative stress during
tumor growth. In the current study, human
glioma U87 cells were transfected with pre-/short hairpin (sh)-PRDX3 vectors and miR-383 mimics/inhibitors. Apoptosis and
reactive oxygen species (ROS) production were detected using flow cytometry. Autophagy was examined using
acridine orange staining, and the expression of cytoplasmic
autophagy-related proteins [
autophagy-related protein 9 (ATG9), Ras-related
protein Rab-1A (Rab1) and p62] was determined using western blot analysis. The interaction between miR-383 and PRDX3 was assessed using a dual-
luciferase assay. The results indicated that both sh-PRDX3 and miR-383 mimics promoted apoptosis and increased the level of mitochondrial ROS, whilst
acridine orange staining revealed that sh-PRDX3 promoted autophagy in U87 cells compared with that in the control cells. The detection of autophagic
proteins indicated that sh-PRDX3 and miR-383 mimics increased the
protein expression level of ATG9 and RAB1, and inhibited that of p62. On the contrary, the effect of miR-383 mimics was opposite to that of pre-PRDX3 in U87 cells. Reverse transcription-quantitative PCR and western blot assays revealed that miR-383 was negatively associated with PRDX3 in U87 cells. miR-383 was indicated to interact with PRDX3, as demonstrated using a dual-
luciferase assay. In conclusion, the present study demonstrated that miR-383 induced cell apoptosis and mitochondrial ROS production by downregulating PRDX3 in U87 cells, thereby promoting oxidative stress-induced autophagy.