Periodontitis leads to irreversible periodontal tissue damage, and current treatments lack sufficient regenerative capacity. This study investigated the role of mmucirc₀000217 in osteogenic differentiation of OCCM-30 cementoblastic cells and its underlying mechanism, aiming to provide a theoretical basis for periodontal tissue regeneration. This study first identified the upregulated expression of mmucirc₀000217 during osteogenic differentiation of OCCM-30 cells using high-throughput sequencing. The impact of mmucirc₀000217 on cell proliferation and apoptosis was evaluated in OCCM-30 cells by modulating its expression and using CCK-8 assays and TUNEL staining. Morphological changes related to mineralization and differentiation were examined using Alkaline Phosphatase (ALP) and Alizarin Red S staining (ARS). Osteogenic gene and protein expressions were analyzed with QPCR and Western blotting, which also detected JAK-STAT3 signaling pathway activation. High-throughput sequencing identified mmucirc₀000217 as the most significantly upregulated circRNA during osteogenic induction. Functional experiments demonstrated that mmucirc₀000217 overexpression significantly enhanced cell proliferation, inhibited apoptosis, and potentiated mineralization, as evidenced by increased ALP activity and Alizarin Red S staining. Conversely, its knockdown produced the opposite effects. Mechanistically, mmucirc₀000217 functioned as a molecular sponge for miR-3064-3p, which led to the derepression of its target, DKK1, and consequent activation of the JAK-STAT3 signaling pathway. Mmucirc₀000217 activated the JAK-STAT3 signaling pathway by adsorbing miR-3064-3p, promoted cell proliferation, inhibited apoptosis, and enhanced osteoblast differentiation. These findings enhance our understanding of the molecular mechanisms behind periodontal tissue regeneration.
Wang et al. (Thu,) studied this question.