miR‐6076 targets BCL6 in SH‐SY5Y cells to regulate amyloid‐β‐induced neuronal damage

Abstract

AbstractAmyloid‐β1‐42 (Aβ1‐42) is strongly associated with Alzheimer's disease (AD). The aim of this study is to elucidate whether and how miR‐6076 participates in the modulation of amyloid‐β (Aβ)‐induced neuronal damage. To construct the neuronal damage model, SH‐SY5Y cells were treated with Aβ1‐42. By qRT‐PCR, we found that miR‐6076 is significantly upregulated in Aβ1‐42‐treated SH‐SY5Y cells. After miR‐6076 inhibition, p‐Tau and apoptosis levels were downregulated, and cell viability was increased. Through online bioinformatics analysis, we found that B‐cell lymphoma 6 (BCL6) was a directly target of miR‐6076 via dual‐luciferase reporter assay. BCL6 overexpression mediated the decrease in elevated p‐Tau levels and increased viability in SH‐SY5Y cells following Aβ1‐42 treatment. Our results suggest that down‐regulation of miR‐6076 could attenuate Aβ1‐42‐induced neuronal damage by targeting BCL6, which provided a possible target to pursue for prevention and treatment of Aβ‐induced neuronal damage in AD.