Research Paper Volume 15, Issue 7 pp 2797—2811

Figure 3. HOXA11-AS competed binding to miR-337-3p to silence miR-337-3p and inhibit apoptotic cell. (A) Neuro-2a cells were transfected with control empty vector or pcDNA3.1-HOXA11-AS vector, and the expression of candidate miRNAs was quantitated by quantitative real-time PCR. (B) Schematic diagram shows the HOXA11-AS transcript binding sites on miR-337-3p. The wild type (WT) and mutated (MUT) binding sites of HOXA11-AS are shown. (C) The luciferase activity of the reporter vectors was detected in Neuro-2a cells at 48 hours after co-transfection of the plasmid expressing wild type or mutant HOXA11-AS together with the NC mimic or the miR-337-3p mimic. (D, E) Neuro-2a cells were transfected with control empty vector or pcDNA3.1-HOXA11-AS vector, and were left untreated or received OGD/R (D). Neuro-2a cells transfected with control sh-RNA or sh-HOXA11-AS were left untreated or treated with 10 μM Dex. Cells were then subjected to OGD/R (E). The relative expression of miR-337-3p was quantitated. (F, G) Neuro-2a cells transfected with control miRNA mimics or miR-337-3p mimics were left untreated or received OGD/R. Cell proliferation (F) and apoptosis (G) in the indicated groups were measured. ^*P < 0.05, ^**P < 0.01, compared with the Control group or between the indicated groups.