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

Abstract

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.