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Published on: February 7, 2025
BBOX1-AS1 ameliorate bone fracture by regulating cell viability and apoptosis of osteoblasts
Ning Liu1, Linkang Du1, Sihan Qu1
1Department of Orthopedics, Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Background:
The main objective of this study was to explore the role of BBOX1-AS1 in the osteogenic differentiation of osteoporosis (OP) and MC3T3-E1 cells.
Methods:
Bone tissue/serum samples from OP-Frx (n = 75), OP-non-Frx (n = 62), and healthy controls (n = 90) were collected. MC3T3-E1 cells were induced for osteogenic differentiation. RT-qPCR detected expression of BBOX1-AS1, miR-134-5p, Follistatin-like 1 (FSTL1), and osteogenic markers (Anxa8, Runx2, Col1a1). Cell viability (CCK-8), alkaline phosphatase (ALP) activity, and apoptosis (flow cytometry) were measured. Dual-luciferase reporter and RNA binding protein immunoprecipitation (RIP) assays verified molecular interactions.
Results:
Compared with controls, BBOX1-AS1 and FSTL1 were significantly upregulated in OP patients, whereas OP-Frx was dramatically upregulated compared with OP-non-Frx, while miR-134-5p was markedly downregulated. Meanwhile, during MC3T3-E1 osteogenic differentiation, BBOX1-AS1 and FSTL1 expression decreased, while miR-134-5p expression increased. Furthermore, silencing of BBOX1-AS1 and FSTL1 promoted cell viability, ALP activity, and Anxa8, Runx2, and Col1a1 levels and reduced apoptosis. Conversely, inhibition of miR-134-5p had an inverse effect. The above data demonstrate that BBOX1-AS1 modulates osteoblast activity and apoptosis by regulating the miR-134-5p/FSTL1 axis.
Conclusion:
Downregulation of BBOX1-AS1 by targeting the miR-134-5p/FSTL1 axis promotes MC3T3-E1 osteogenic differentiation. Our study opens up new avenues for the diagnosis and treatment of osteoporotic fractures.
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