Abstract
The present study aimed to examine how the long non‑coding RNA (lncRNA) RP11‑543N12.1 interacted with microRNA (miR)‑324‑3p to modify microglials (MIs)‑induced neuroblastoma cell apoptosis, which may pose benefits to the treatment of Alzhemier's disease (AD). The cell model of AD was established by treating SH‑SY5Y cells with amyloid β (Aβ)25‑35, and MI were acquired using primary cell culture technology. The lncRNAs that were differentially expressed between SH‑SY5Y and control cells were screened through a microarray assay and confirmed via polymerase chain reaction. In addition, overexpression of RP11‑543N12.1 and miR‑324‑3p was established by transfection of SH‑SY5Y cells with pcDNA3.1(+)‑RP11‑543N12.1 and miR‑324‑3p mimics, respectively, while downregulation of RP11‑543N12.1 and miR‑324‑3p was achieved by transfection with RP11‑543N12.1‑small interfering RNA (siRNA) and miR‑324‑3p inhibitor, respectively. The interaction between RP11‑543N12.1 and miR‑324‑3p was confirmed with a dual‑luciferase reporter gene assay. The results revealed that the expression levels of total and phosphorylated tau in SH‑SY5Y cells were significantly elevated following Aβ25‑35 treatment (P<0.05), and RP11‑543N12.1 was found to be differentially expressed between the control and Aβ25‑35‑treated cells (P<0.05). Furthermore, the targeted association of RP11‑543N12.1 and miR‑324‑3p was predicted based on miRDB4.0 and PITA databases, and then validated via the dual‑luciferase reporter gene assay. SH‑SY5Y cells transfected with siRNA or inhibitor, and treated with Aβ25‑35 displayed cellular survival and apoptosis that were similar to the normal levels (P<0.05). Finally, co‑culture of MI and SH‑SY5Y cells transfected with RP11‑543N12.1‑siRNA/miR‑324‑3p inhibitor significantly enhanced cell apoptosis (P<0.05). In conclusion, RP11‑543N12.1 targeted miR‑324‑3p to suppress proliferation and promote apoptosis in the AD cell model, suggesting that RP11‑543N12.1 and miR‑324‑3p may be potential biomarkers and therapeutic targets for AD.