Background: This study aimed to investigate the role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms, in osteoarthritis (OA). Methods: Cartilage tissues of OA patients and healthy volunteers were isolated and cultured. After transfection with the appropriate constructs, chondrocytes were classified into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics groups. qRT-PCR was used to detect the expression of MEG3, miR-361-5p and FOXO1. Western blot, luciferase reporter assay, RIP, CCK-8, and flow cytometry analysis were performed to reveal the morphology, proliferation, and apoptotic status of cartilage cells. Histological analysis and immunostaining were conducted in the OA rat model.Results: Expression of MEG3 and FOXO1 was significantly decreased in OA compared with the normal group, while the expression of miR-361-5p was increased. MEG3 might serve as a ceRNA of miR-361-5p in OA chondrocytes. Moreover, using western blot analyses and the CCK-8 assay, MEG3 was shown to target miR-361-5p/FOXO1, elevate cell proliferation, and impair cell apoptosis. Functional analysis in vivo showed that MEG3 suppressed degradation of the cartilage matrix. Conclusion: MEG3 can contribute to cell proliferation and inhibit cell apoptosis and degradation of extracellular matrix (ECM) via the miR-361-5p/FOXO1 axis in OA chondrocytes.

Background: This study aimed to investigate the role of long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were involved in OA group and control group, respectively. Cartilage tissues of all patients were isolated and cultured. Based on different transfection, MEG3 cells were grouped into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics group. The cells transfected with pcDNA3.1-NC and pcDNA3.1-MEG3, and then cultured with XAV939 was named as pcDNA3.1-NC +XAV939 group and pcDNA3.1-MEG3 + XAV939 group respectively. The RT-qPCR was used to detect the expression of MEG3 and miR-361-5p . Moreover, Western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis in cartilage cells. Finally, the histological analysis and immunostaining were performed on OA rat model. Results: The expression of lncRNA MEG3 and miR-361-5p in OA was significantly decreased and increased respectively than that in normal. Meanwhile, MEG3 was competitive binding with miR-361-5p in OA chondrocytes. Moreover, the Western blot and CCK-8 assay showed that MEG3 might inhibit cell proliferation and promote cell apoptosis via Wnt/β-catenin pathway. Finally, rat model analysis showed that MEG3 contributed to the cartilage matrix degradation. Conclusion: MEG3 and miR-361-5p might down-regulated and up-regulated respectively in the chondrocytes of OA patients. Furthermore, MEG3 might inhibit cell proliferation and promote cell apoptosis via miR-361-5p/Wnt/β-catenin axis in OA chondrocytes.