Chen Zhiqing, Liu Zhi, Shen Lin, Jiang Han
Department of Osteology, Tianjin Third Central Hospital Tianjin 300170, China.
Tianjin Institute of Hepatobiliary Disease Tianjin 300170, China.
Am J Transl Res. 2019 Feb 15;11(2):974-982. eCollection 2019.
Fracture is the most common disease in the orthopedics. Long non-coding small nucleolar RNA host gene 7 (SNHG7) has been confirmed to enhance cell proliferation and decrease cell apoptosis in many cancers. However, the role of SNHG7 in skeletal fracture remains largely to be elucidated. In the current study, we observed SNHG7 was down-regulated in femoral neck fracture tissues. In addition, SNHG7 knockdown inhibited proliferation and migration, induced apoptosis, reduced activity in osteoblast cells in vitro. Bioinformatics analysis revealed SNHG7 acts as a molecular sponge for miR-9 and MiR-9 directly targets with 3'-UTR of TGFBR2. Furthermore, SNHG7 knockdown repressed the TGF-β signaling pathway. Taken together, this study manifested SNHG7 promotes bone repair in femoral neck fracture, and may serve as a potential target for enhancing bone formation.
骨折是骨科最常见的疾病。长链非编码小核仁RNA宿主基因7（SNHG7）已被证实在许多癌症中可增强细胞增殖并减少细胞凋亡。然而，SNHG7在骨骼骨折中的作用仍有待进一步阐明。在本研究中，我们观察到SNHG7在股骨颈骨折组织中表达下调。此外，SNHG7基因敲低抑制了体外成骨细胞的增殖和迁移，诱导了细胞凋亡，降低了细胞活性。生物信息学分析显示，SNHG7作为miR-9的分子海绵，而miR-9直接靶向TGFBR2的3'-UTR。此外，SNHG7基因敲低抑制了TGF-β信号通路。综上所述，本研究表明SNHG7促进股骨颈骨折的骨修复，并可能成为促进骨形成的潜在靶点。
