Bone · 2026
LncRNA FGF13-AS1 predicts delayed fracture healing and promotes osteoporotic fracture healing by regulating miR-128-3p/CBFB-mediated osteogenesis and osteoclast activity.
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Yao Shanchuan, Meng Jiande, Qin Zhou, Zhang Yuanyuan
Аннотация
OBJECTIVE: Osteoporotic fracture (OPF) disrupts bone homeostasis via resorption-formation imbalance. This study investigates the expression and role of the long non-coding RNA FGF13 antisense RNA 1 (FGF13-AS1) in OPF bone healing.
METHODS: Recruited 110 patients with osteoporosis (OP) and 138 patients with OPF and 90 healthy people, then divided OPF patients into normal healing (NFH) and delayed healing groups (DFH) after a 4-month follow-up. In vitro, MC3T3-E1 cells undergo osteogenic differentiation while RAW264.7 cells undergo osteoclastogenic differentiation. Serum FGF13-AS1 and miR-128-3p levels were determined by real-time quantitative reverse transcription PCR (RT-qPCR). The receiver operating characteristic (ROC) curve assessed FGF13-AS1's diagnostic value for OP. Logistic regression pinpointed potential risk factors for DFH. Cell counting kit-8 (CCK-8) and flow cytometry assays were used to determine cell proliferation and apoptosis. Alkaline phosphatase (ALP) and tartrate-resistant acid phosphatase (TRAP) activity were measured via commercial kits. RT-qPCR evaluated expression of osteogenic and osteoclast differentiation markers.
RESULTS: Serum FGF13-AS1 levels decline significantly in OP patients, particularly in OPF cases. DFH patients have lower levels than NFH patients. Low FGF13-AS1 expression predicts DFH and is a potential risk factor for its onset. MC3T3-E1 cells in osteoblastic differentiation showed marked upregulation of FGF13-AS1 and core-binding factor subunit β (CBFB) and downregulation of miR-128-3p. FGF13-AS1 overexpression enhanced ALP activity, osteogenic marker expression, and cell proliferation, and suppressed apoptosis; miR-128-3p effectively reversed these effects. During osteoclast differentiation, FGF13-AS1 and CBFB decreased, and miR-128-3p increased. Inhibition of FGF13-AS1 elevated TRAP activity and osteoclast differentiation markers. This effect was markedly mitigated by reducing miR-128-3p levels.
CONCLUSION: Low FGF13-AS1 serves as a marker for delayed fracture healing in osteoporosis. It likely acts via the miR-128-3p/CBFB axis to balance osteogenic differentiation and promote bone formation. Deficiency of FGF13-AS1 may contribute to delayed healing and represents a potential clinical molecular target.
METHODS: Recruited 110 patients with osteoporosis (OP) and 138 patients with OPF and 90 healthy people, then divided OPF patients into normal healing (NFH) and delayed healing groups (DFH) after a 4-month follow-up. In vitro, MC3T3-E1 cells undergo osteogenic differentiation while RAW264.7 cells undergo osteoclastogenic differentiation. Serum FGF13-AS1 and miR-128-3p levels were determined by real-time quantitative reverse transcription PCR (RT-qPCR). The receiver operating characteristic (ROC) curve assessed FGF13-AS1's diagnostic value for OP. Logistic regression pinpointed potential risk factors for DFH. Cell counting kit-8 (CCK-8) and flow cytometry assays were used to determine cell proliferation and apoptosis. Alkaline phosphatase (ALP) and tartrate-resistant acid phosphatase (TRAP) activity were measured via commercial kits. RT-qPCR evaluated expression of osteogenic and osteoclast differentiation markers.
RESULTS: Serum FGF13-AS1 levels decline significantly in OP patients, particularly in OPF cases. DFH patients have lower levels than NFH patients. Low FGF13-AS1 expression predicts DFH and is a potential risk factor for its onset. MC3T3-E1 cells in osteoblastic differentiation showed marked upregulation of FGF13-AS1 and core-binding factor subunit β (CBFB) and downregulation of miR-128-3p. FGF13-AS1 overexpression enhanced ALP activity, osteogenic marker expression, and cell proliferation, and suppressed apoptosis; miR-128-3p effectively reversed these effects. During osteoclast differentiation, FGF13-AS1 and CBFB decreased, and miR-128-3p increased. Inhibition of FGF13-AS1 elevated TRAP activity and osteoclast differentiation markers. This effect was markedly mitigated by reducing miR-128-3p levels.
CONCLUSION: Low FGF13-AS1 serves as a marker for delayed fracture healing in osteoporosis. It likely acts via the miR-128-3p/CBFB axis to balance osteogenic differentiation and promote bone formation. Deficiency of FGF13-AS1 may contribute to delayed healing and represents a potential clinical molecular target.