Qian Jin, Ge Lujie, Lu Congcong, Han Xiao, Li Maoqiang, Bian Zhenyu
Department of Orthopedics, Affiliated Hangzhou First People's Hospital, WestLake University School of Medicine, Hangzhou 310006, Zhejiang Province, China.
Department of Orthopedics, Affiliated Hangzhou First People's Hospital, WestLake University School of Medicine, Hangzhou 310006, Zhejiang Province, China.
Int J Biol Macromol. 2024 Sep 16;280(Pt 1):135727. doi: 10.1016/j.ijbiomac.2024.135727.
Long non-coding RNAs (lncRNAs) have been demonstrated to participate in a variety of physiological and pathological processes, including tumor initiation and development. Nevertheless, few of them have been investigated in chondrosarcoma. Here, we were intended to unveil the role of long intergenic non-protein coding RNA 665 (LINC00665) in chondrosarcoma. RT-qPCR was adopted for gene expression detection. The biological processes in chondrosarcoma cells were detected by CCK-8, EdU, TUNEL, Transwell and wound healing assays. The relationships between genes in chondrosarcoma cells were evaluated by a series of mechanism experiments including RIP, luciferase reporter assays and so on.LINC00665 expressed at a high level in chondrosarcoma cell lines. LINC00665 interference suppressed cell proliferation, migration and invasion in chondrosarcoma. Besides, LINC00665 interacted with microRNA-665 (miR-665), which was then verified to be down-regulated in chondrosarcoma cells. Additionally, LINC00665 and miR-665 were mutually inhibited by each other in chondrosarcoma cells. Importantly, LINC00665 stimulated fibroblast growth factor 9 (FGF9) expression in chondrosarcoma cells via sponging miR-665. Furthermore, FGF9 participated in the regulation of LINC00665-promoted chondrosarcoma development. CONCLUSION: LINC00665 facilitates chondrosarcoma progression via miR-665/FGF9 axis, which might indicate a new path for the treatment of chondrosarcoma.
长链非编码RNA（lncRNAs）已被证明参与多种生理和病理过程，包括肿瘤的发生和发展。然而，在软骨肉瘤中对它们的研究较少。在此，我们旨在揭示长链基因间非编码RNA 665（LINC00665）在软骨肉瘤中的作用。采用RT-qPCR检测基因表达。通过CCK-8、EdU、TUNEL、Transwell和伤口愈合实验检测软骨肉瘤细胞中的生物学过程。通过一系列机制实验，包括RIP、荧光素酶报告基因检测等，评估软骨肉瘤细胞中基因之间的关系。LINC00665在软骨肉瘤细胞系中高表达。LINC00665干扰可抑制软骨肉瘤细胞的增殖、迁移和侵袭。此外，LINC00665与微小RNA-665（miR-665）相互作用，随后证实miR-665在软骨肉瘤细胞中表达下调。此外，在软骨肉瘤细胞中LINC00665和miR-665相互抑制。重要的是，LINC00665通过吸附miR-665刺激软骨肉瘤细胞中纤维母细胞生长因子9（FGF9）的表达。此外，FGF9参与了LINC00665促进的软骨肉瘤发展的调控。结论：LINC00665通过miR-665/FGF9轴促进软骨肉瘤进展，这可能为软骨肉瘤的治疗指明一条新途径。
