The long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) plays a crucial role in tumorigenesis and is frequently employed as a prognostic biomarker. However, its involvement in the osteogenic differentiation of oral stem cells, particularly human dental follicle stem cells (hDFSCs), remains unclear. Our investigation revealed that the absence of SNHG1 enhances the osteogenic differentiation of hDFSCs. Furthermore, the downregulation of SNHG1 induces autophagy in hDFSCs, leading to a reduction in intracellular oxidative stress levels. Notably, this effect is orchestrated through the epigenetic regulation of EZH2. Our study unveils a novel function of SNHG1 in governing the osteogenic differentiation of hDFSCs, offering fresh insights for an in‐depth exploration of the molecular mechanisms underlying dental follicle development. These findings not only provide a foundation for advancing the understanding of SNHG1 but also present innovative perspectives for promoting the repair and regeneration of periodontal supporting tissue, ultimately contributing to the restoration of periodontal health and tooth function.

中文翻译：

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SNHG1敲低通过自噬介导的抗氧化应激促进hDFSCs的成骨分化

长非编码 RNA (lncRNA) 小核仁 RNA 宿主基因 1 (SNHG1) 在肿瘤发生中发挥着至关重要的作用，经常被用作预后生物标志物。然而，其在口腔干细胞，特别是人牙囊干细胞（hDFSC）的成骨分化中的作用仍不清楚。我们的研究表明，SNHG1 的缺失增强了 hDFSC 的成骨分化。此外，SNHG1 的下调会诱导 hDFSC 中的自噬，从而导致细胞内氧化应激水平降低。值得注意的是，这种效应是通过 EZH2 的表观遗传调控来协调的。我们的研究揭示了 SNHG1 在控制 hDFSC 成骨分化中的新功能，为深入探索牙囊发育的分子机制提供了新的见解。这些发现不仅为加深对SNHG1的理解奠定了基础，而且为促进牙周支持组织的修复和再生提供了创新视角，最终有助于牙周健康和牙齿功能的恢复。