Down-regulation of long noncoding RNA HOXA11-AS nullifies the impact of microRNA-506–3p on chondrocytes proliferation and apoptosis in osteoarthritis

•HOXA11-AS silencing restrained HCOA cell proliferation and accelerated their apoptosis.•HOXA11-AS overexpression increased PIK3CA expression through binding to miR-506–3p.•HOXA11-AS overexpression represses PI3K/AKT/mTOR pathway through miR-506–3p down-regulation. This study was directed towards exploring the impacts of lncRNA HOXA11-AS-mediated microRNA (miR)-506–3p on chondrocytes proliferation and apoptosis in osteoarthritis (OA). The articular cartilages were provided by OA patients who received total knee arthroplasty, and Human Chondrocyte (HC)-OA (HCOA) was also attained. The miR-506–3p and HOXA11-AS expressions in articular cartilages from OA patients and HCOA cells were analyzed via qPCR. After gain- and loss-of-function assays in HCOA cells, MTT assay and flow cytometry (FC) were used for assessing cell viability and apoptosis, accordingly. The levels of PIK3CA, AKT, and mTOR as well as AKT and mTOR phosphorylation levels assessed using western blotting (WB). The targeting correlation of HOXA11-AS and miR-506–3p as well as miR-506–3p and PIK3CA was assessed through Dual-Luciferase Reporter gene Assay (DLRA). The articular cartilages from OA patients and Human Chondrocyte (HC)-OA (HCOA) cells showed increased HOXA11-AS and decreased miR-506–3p. Mechanistically, HOXA11-AS was capable of binding to miR-506–3p to increase PIK3CA, the target gene of miR-506–3p. miR-506–3p suppression facilitated HCOA cell proliferation and reduced their apoptosis, which was nullified by further silencing HOXA11-AS or silencing PIK3CA. The down-regulation of HOXA11-AS disrupted the PI3K/AKT/mTOR pathway, which was counteracted by further miR-506–3p inhibition. The silencing of HOXA11-AS might block the PI3K/AKT/mTOR pathway through miR-506–3p up-regulation, thereby restricting HCOA cell proliferation and provoking apoptosis.