Osteoporosis is one of the most prevailing orthopedic diseases that causes a heavy burden on public health. Given that bone marrow-derived mesenchymal stem cells (BMSCs) are of immense importance in osteoporosis development, it is necessary to expound the mechanisms underlying BMSC osteoblastic differentiation. Although mounting research works have investigated the role of small nucleolar RNA host gene 5 (SNHG5) in various diseases, elucidations on its function in osteoporosis are still scarce. It was observed that SNHG5 and RUNX family transcription factor 3 (RUNX3) were remarkably elevated during osteogenic differentiation of human bone marrow mesenchymal stem cells (hBMSCs). Further, we disclosed that the silencing of SNHG5 suppressed osteogenic differentiation and induced apoptosis of hBMSCs. What's more, SNHG5 acted as a competing endogenous RNA to affect RUNX3 expression via competitively binding with microRNA (miR)-582-5p. RUNX3 was also confirmed to simulate the transcriptional activation of SNHG5. Finally, our findings manifested that the positive feedback loop of SNHG5/miR-582-5p/RUNX3 executed the promoting role in the development of osteoporosis, which shed light on specific molecular mechanism governing SNHG5 in osteogenic differentiation and apoptosis of hBMSCs and indicated that SNHG5 may represent a novel target for the improvement of osteoporosis therapy.
Keywords: RUNX3; SNHG5; lncRNA; miR-582-5p; osteoporosis.
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