OBJECTIVE: Long noncoding RNAs (lncRNAs) have been reported to participate in many diseases. Fracture healing is one of these ordinary diseases. This study aims to identify how lncRNA HOXA11-AS affects the progression of fracture healing. MATERIALS AND METHODS: RT-qPCR was performed to detect the level of HOXA11-AS. Moreover, function assays including cell growth assay and cell apoptosis assay were performed to explore how HOXA11-AS functions in fracture healing. Furthermore, the interaction between HOXA11-AS and mir-124-3p was studied by RT-qPCR, luciferase assay, and RNA immunoprecipitation assay. Rescue experiments were performed to verify the interaction between HOXA11-AS and mir-124-3p in vitro. RESULTS: In the research, function assays revealed that HOXA11-AS overexpression inhibited cell proliferation, while HOXA11-AS knockdown promoted cell proliferation in vitro. Moreover, HOXA11-AS overexpression promoted cell apoptosis, while HOXA11-AS knockdown inhibited cell apoptosis in vitro. Furthermore, mechanism assays demonstrated that HOXA11-AS acts a ceRNA via sponging mir-124-3p. Rescue assay demonstrated that HOXA11-AS suppressed cell proliferation and promoted cell apoptosis via targeting mir-124-3p. CONCLUSIONS: These results indicate that HOXA11-AS could inhibit cell proliferation and promote cell apoptosis of osteoblast via sponging mir-124-3p, which may offer a new vision for interpreting the mechanism of fracture healing.
OBJECTIVE: Long noncoding RNAs (lncRNAs) have been reported to participate in many diseases. Fracture healing is one of these ordinary diseases. This study aims to identify how lncRNA HOXA11-AS affects the progression of fracture healing. MATERIALS AND METHODS: RT-qPCR was performed to detect the level of HOXA11-AS. Moreover, function assays including cell growth assay and cell apoptosis assay were performed to explore how HOXA11-AS functions in fracture healing. Furthermore, the interaction between HOXA11-AS and mir-124-3p was studied by RT-qPCR, luciferase assay, and RNA immunoprecipitation assay. Rescue experiments were performed to verify the interaction between HOXA11-AS and mir-124-3p in vitro. RESULTS: In the research, function assays revealed that HOXA11-AS overexpression inhibited cell proliferation, while HOXA11-AS knockdown promoted cell proliferation in vitro. Moreover, HOXA11-AS overexpression promoted cell apoptosis, while HOXA11-AS knockdown inhibited cell apoptosis in vitro. Furthermore, mechanism assays demonstrated that HOXA11-AS acts a ceRNA via sponging mir-124-3p. Rescue assay demonstrated that HOXA11-AS suppressed cell proliferation and promoted cell apoptosis via targeting mir-124-3p. CONCLUSIONS: These results indicate that HOXA11-AS could inhibit cell proliferation and promote cell apoptosis of osteoblast via sponging mir-124-3p, which may offer a new vision for interpreting the mechanism of fracture healing.