lncRNA SNHG1 attenuates osteogenic differentiation via the miR‑101/DKK1 axis in bone marrow mesenchymal stem cells.

The imbalance induced by inhibition of bone mesenchymal stem cell (BMSC) osteogenic differentiation results in osteoporosis (OP); however, the underlying regulatory mechanism is not completely understood. Long non‑coding RNAs (lncRNAs) serve crucial roles in osteogenic differentiation; therefore, investigating their regulatory role in the process of osteogenic differentiation may identify a promising therapeutic target for OP. The expression of small nucleolar RNA host gene 1 (SNHG1), Dickkopf 1 (DKK1), microRNA (miR)‑101, RUNX family transcription factor 2 (RUNX2), osteopontin (OPN) and osteocalin (OCN) were detected via reverse transcription‑quantitative PCR. The protein expression levels of DKK1, β‑catenin, RUNX2, OPN, OCN, osterix and collagen type I α1 chain were analyzed by performing western blotting. The osteoblastic phenotype was assessed by conducting alkaline phosphatase activity detection and Alizarin Red staining. The interaction between SNHG1 and miR‑101 was validated by bioinformatics and luciferase assays. The regulatory role of SNHG1 in BMSC osteogenic differentiation was assessed. SNHG1 expression was downregulated in a time‑dependent manner during the process of osteogenic differentiation. SNHG1 overexpression inhibited osteogenic differentiation compared with the pcDNA group. The results indicated that SNHG1 and DKK1 directly interacted with miR‑101. Moreover, SNHG1 regulated the Wnt/β‑catenin signaling pathway to inhibit osteogenic differentiation via the miR‑101/DKK1 axis. The present study indicated that lncRNA SNHG1 could attenuate BMSC osteogenic differentiation via the miR‑101/DKK1 axis as a competitive endogenous RNA. Therefore, the present study furthered the current understanding of the potential mechanism underlying lncRNAs in in osteogenic differentiation.