Background
BMSCs with robust osteogenic differentiation capacity can participate in the repair of osteoporotic (OP) bone. Long non-coding RNAs (LncRNAs) serve as crucial regulators of osteogenic differentiation. This study aims to investigate the clinical implications of LINC00968 in OP and elucidate its molecular mechanisms.
Conclusions
Our results indicate that LINC00968 downregulation is a diagnostic biomarker for OP, facilitating osteogenic differentiation and inhibiting apoptosis via miR-17-5p/STAT3 axis, suggesting a new therapeutic target for OP progression.
Methods
Patients with OP and controls without OP were enrolled. RT-qPCR was utilized the quantify the levels of LINC00968, miR-17-5p, STAT3, and osteogenic differentiation markers. ROC curve was conducted to evaluate the diagnostic significance. Osteogenic differentiation medium (OM) induced hBMSCs. Flow cytometry was used to examine apoptosis. DLR and RIP assay were performed to validate target binding.
Results
LINC00968 was notably decreased in the serum and bone tissue of patients with OP, whereas it was markedly elevated during osteogenic differentiation of hBMSCs. LINC00968 has 78.65% sensitivity and 71.95% specificity in identifying OP patients from controls. Silencing of LINC00968 sharply diminished ALP activity and osteogenic differentiation markers levels while promoting apoptosis in hBMSCs under OM induction. However, this reduction was notably reversed by the administration of a miR-17-5p inhibitor. Molecularly, miR-17-5p directly targets LINC00968 and STAT3. Conclusions: Our results indicate that LINC00968 downregulation is a diagnostic biomarker for OP, facilitating osteogenic differentiation and inhibiting apoptosis via miR-17-5p/STAT3 axis, suggesting a new therapeutic target for OP progression.