MicroRNA-20b-5p aggravates neuronal apoptosis induced by β-Amyloid via down-regulation of Ras homolog family member C in Alzheimer’s disease

•Upregulated miR-20b-5p and downregulated RhoC in hippocampus of APPswe/PSΔE9 mice.•miR-20b-5p inhibitor reduces the neuronal toxicity induced by Aβ25−35.•miR-20b-5p suppresses RhoC expression via targeting 3′-UTR of RhoC mRNA.•Inhibited miR-20b-5p reverses effects of downregulated RhoC on neuronal toxicity. Recent studies have reported that microRNAs are abnormally expressed in brain tissues of Alzheimers disease (AD) patients. However, the accurate function of miR-20b-5p in AD has not been elucidated. We intended to investigate the role and underlying mechanism of miR-20b-5p in AD. The expression of miR-20b-5p was increased, and the expression of RhoC was decreased in the hippocampus of Appswe/PS△E 9 mice. In order to construct a cell model in vitro to study the underlying action mechanism, PC12 cells were treated with Aβ25−35. The cell apoptosis detected by flow cytometry and the expression of cleaved-caspase-3 detected by western blot were both remarkably increased in PC12 cells treated with Aβ25−35, but they were reduced by miR-20b-5p inhibitor. In addition, MTT test showed that the cell survival rate in Aβ25−35 + miR-20b-5p inhibitor group was higher than that in Aβ25−35 + NC inhibitor group. Double luciferase reporter gene analysis confirmed that the binding site of miR-20b-5p was in 3′- UTR of RhoC mRNA. Knockdown of RhoC increased neuronal apoptosis induced by Aβ25−35 and the expression of cleaved-caspase-3, while miR-20b-5p inhibitor reversed these effects. Knockdown of RhoC aggravated the inhibition effect on cell viability induced by Aβ25−35, while miR-20b-5p inhibitor diminished these effects. In conclusion, inhibition of miR-20b-5p attenuates apoptosis induced by Aβ25−35 in PC12 cells through targeting RhoC. Therefore, miR-20b-5p may be a perspective curative target for AD.