Expression of LINC00511 is associated with postmenopausal osteoporosis and modulates early osteogenic events in pre-osteoblasts via the miR-150-5p/RAD51 axis

Abstract Background Post-menopausal osteoporosis (PMOP) is a common metabolic skeletal disorder associated with reduced quality of life and increased mortality. Objectives This study aimed to explore the potential auxiliary diagnostic value of LINC00511 in PMOP and examine the regulation of early osteogenic events in pre-osteoblasts by the Linc00511/miR-150-5p/RAD51 axis. Materials and methods This study enrolled 122 controls and 126 PMOP. RT-PCR was utilised to assess the expression levels of LINC00511 ,RUNX2 and ALP. A multivariate logistic regression and ROC analysis evaluated LINC00511 ’s predictive value for PMOP. Pearson correlation linked LINC00511 to bone turnover markers. CCK-8 and Annexin-V/PI assays assessed its effects on osteoblast proliferation and apoptosis. Bioinformatics, luciferase reports, and RIP assays confirmed the miR-150-5p interaction with Linc00511 and RAD51. Results In PMOP patients, serum LINC00511 levels were significantly lower than those in healthy postmenopausal women. LINC00511 abundance was positively correlated with T-scores and site-specific bone mineral density. A detectable decline in LINC00511 independently predicted PMOP patient’s onset and conferred high diagnostic accuracy for the disorder. Overexpression of linc00511 promoted proliferation and early osteogenic events, and repressed apoptosis in MC3T3-E1 cells. By contrast, lncRNA depletion induced the opposite phenotypic changes. Inhibition of miR-150-5p reversed the cellular injury evoked by linc00511 deletion, whereas this rescue phenotype was subsequently abrogated upon further silencing of RAD51. Conclusion LINC00511 may be an indicator for diagnosing PMOP patients, and the linc00511 /miR-150-5p/RAD51 axis may participate in regulating early osteogenic events, suggesting its possible relevance to osteoporosis progression.