Chinese Journal of Tissue Engineering Research ›› 2025, Vol. 29 ›› Issue (5): 899-907.doi: 10.12307/2025.281

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MiR-338-3p affects proliferation and apoptosis of alveolar bone osteoblasts by targeting receptor activator of nuclear factor-kappaB ligand 

Lang Mecuo, Zhang Yilin, Wang Li   

  • Received:2023-12-01 Accepted:2024-02-07 Online:2025-02-18 Published:2024-06-01
  • Contact: Lang Mecuo, Department of Stomatology, The First People’s Hospital of Shuangliu District (West China Airport Hospital of Sichuan University), Chengdu 621000, Sichuan Province, China​
  • About author:Lang Mecuo, Master, Associate chief physician, Department of Stomatology, The First People’s Hospital of Shuangliu District (West China Airport Hospital of Sichuan University), Chengdu 621000, Sichuan Province, China

Abstract:

BACKGROUND: MiR-338-3p could inhibit osteoclast differentiation, and downregulation of receptor activator of nuclear factor-κB ligand level could promote bone formation. However, it is unclear whether miR-338-3p can affect the proliferation and apoptosis of alveolar bone osteoblasts by regulating the receptor activator of nuclear factor-κB ligand level.
OBJECTIVE: To explore the effect and mechanism of miR-338-3p on proliferation and apoptosis of alveolar bone osteoblasts by targeting receptor activator of nuclear factor-κB ligand. 
METHODS: Human alveolar bone osteoblasts were isolated, transfected and treated with Wnt-C59 (Wnt/β-catenin pathway inhibitor), and divided into transfection control group, miR-338-3p group, miR-338-3p+control group, miR-338-3p+receptor activator of nuclear factor-κB ligand group and miR-338-3p+Wnt-C59 group. The dual luciferase report experiment was used to verify the regulatory effect of miR-338-3p on receptor activator of nuclear factor-κB ligand. Cell counting kit-8 and 5-Ethynyl-2’-deoxyuridine staining were used to detect cell proliferation levels. Flow cytometry was used to detect cell cycle and apoptosis levels. RT-qPCR was used to detect miR-338-3p, receptor activator of nuclear factor-κB ligand, Wnt-3a, β-Catenin, glycogen synthase kinase-3β mRNA levels. Western blot was used to detect RANKL, proliferating cell nuclear antigen, Ki67, CyclinD1, B-cell lymphoma/leukemia-2, B-cell lymphoma-2 related X protein, Caspase3, Wnt-3a, β-catenin, glycogen synthase kinase-3β protein levels. 
RESULTS AND CONCLUSION: miR-338-3p could target the regulation of receptor activator of nuclear factor-κB ligand. After overexpression of miR-338-3p, cell survival rate, 5-Ethynyl-2’-deoxyuridine positive cell rate, proportion of S-phase cells were increased, and apoptosis rate was decreased. The mRNA and protein levels of miR-338-3p, proliferating cell nuclear antigen, Ki67, CyclinD1, B-cell lymphoma/leukemia-2, Wnt-3a, and β-catenin were increased, while the mRNA and protein levels of B-cell lymphoma-2 related X protein, Caspase3 protein, receptor activator of nuclear factor-κB ligand, and glycogen synthase kinase-3β were decreased (all P < 0.05). Overexpression of receptor activator of nuclear factor-κB ligand or Wnt-C59 could weaken the effects of overexpression of miR-338-3p on cell proliferation and apoptosis (all P < 0.05). Overall, miR-338-3p promotes alveolar bone osteoblast proliferation and inhibits apoptosis by targeting receptor activator of nuclear factor-κB ligand, which may act through activation of the Wnt/β-catenin signaling pathway.

Key words: miR-338-3p, receptor activator of nuclear factor-κB ligand, alveolar bone osteoblast, Wnt/β-catenin signaling pathway

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