Li Zhuokai, Wang Xiaohe, Liang Shuofu
Department of Orthopaedics, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai 201318, P.R. China.
Department of Orthopaedics, Jinan Zhangqiu District Hospital of TCM, Jinan, Shandong 250200, P.R. China.
Exp Ther Med. 2021 Apr;21(4):325. doi: 10.3892/etm.2021.9756. Epub 2021 Feb 5.
The aim of the present study was to clarify the effect of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) on the proliferation, migration and invasion of osteosarcoma (OS) cells and to explore the potential underlying mechanisms. The expression levels of SNHG1, microRNA (miR)-424-5p and fibroblast growth factor 2 (FGF2) in OS tissues and cells were detected using reverse transcription-quantitative polymerase chain reaction. OS cell proliferation, migration and invasion were analysed by MTT, wound healing and Transwell invasion assays, respectively. The targeting relationships between SNHG1 and miR-424-5p, as well as between miR-424-5p and FGF2, were confirmed using RNA-binding protein immunoprecipitation and/or dual-luciferase reporter gene assays. The results demonstrated that the expression levels of SNHG1 and FGF2 were upregulated, whereas the expression of miR-424-5p was downregulated in OS tissues and cells. The silencing of SNHG1 significantly inhibited the proliferation, migration and invasion of OS cells. Additionally, FGF2 was shown to be a target of miR-424-5p, which in turn, was a target of SNHG1. miR-424-5p silencing and FGF2 overexpression both reversed the suppressive effects of SNHG1 knockdown on the proliferation, migration and invasion of OS cells. Thus, the silencing of SNHG1 may inhibit the proliferation, migration and invasion of OS cells by regulating the miR-424-5p/FGF2 axis.
本研究旨在阐明长链非编码RNA(lncRNA)小核仁RNA宿主基因1(SNHG1)对骨肉瘤(OS)细胞增殖、迁移和侵袭的影响,并探讨其潜在的作用机制。采用逆转录-定量聚合酶链反应检测OS组织和细胞中SNHG1、微小RNA(miR)-424-5p和成纤维细胞生长因子2(FGF2)的表达水平。分别通过MTT、伤口愈合和Transwell侵袭实验分析OS细胞的增殖、迁移和侵袭能力。采用RNA结合蛋白免疫沉淀和/或双荧光素酶报告基因实验证实SNHG1与miR-424-5p以及miR-424-5p与FGF2之间的靶向关系。结果表明,OS组织和细胞中SNHG1和FGF2的表达水平上调,而miR-424-5p的表达下调。沉默SNHG1可显著抑制OS细胞的增殖、迁移和侵袭。此外,FGF2是miR-424-5p的靶点,而miR-424-5p又是SNHG1的靶点。沉默miR-424-5p和过表达FGF2均可逆转SNHG1敲低对OS细胞增殖、迁移和侵袭的抑制作用。因此,沉默SNHG1可能通过调节miR-424-5p/FGF2轴抑制OS细胞的增殖、迁移和侵袭。