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通过miR-665/FGF9通路,LINC00665会加剧软骨肉瘤细胞中的恶性表型
Jin Qian1, Lujie Ge1, Congcong Lu1
1Department of Orthopedics, Affiliated Hangzhou First People's Hospital, WestLake University School of Medicine, Hangzhou 310006, Zhejiang Province, China.
International journal of biological macromolecules
|September 18, 2024
概括
长跨基因非蛋白编码RNA 665 (LINC00665) 通过与microRNA-665 (miR-665) 和纤维细胞生长因子9 (FGF9) 相互作用,促进了软骨肉瘤的进展. 这一轴为软骨肉瘤治疗提供了潜在的新治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 长非编码RNAs (lncRNAs) 与瘤发生有关,但它们在冠状动脉瘤中的作用在很大程度上仍未被探索.
- 软骨肉瘤是一种罕见的骨癌,有效的治疗选择有限.
研究的目的:
- 调查长跨基因非蛋白质编码RNA 665 (LINC00665) 在软骨肉瘤的发展和进展中的作用.
- 阐明LINC00665在软骨肉瘤中的功能背后的分子机制.
主要方法:
- 定量实时PCR (RT-qPCR) 用于基因表达分析.
- 细胞增殖 (CCK-8,EDU),细胞亡 (TUNEL),迁移和入侵试验 (Transwell,伤口愈合).
- RNA免疫沉 (RIP),光酶记者试验,以探索分子相互作用.
主要成果:
- 在冠状腺癌细胞系中,LINC00665的调节显著上升.
- LINC00665干扰抑制了冠状腺癌细胞的增殖,迁移和入侵.
- LINC00665充当了microRNA-665 (miR-665) 的海绵,导致纤维细胞生长因子9 (FGF9) 表达的增加,这推动了软骨肉瘤的进展.
结论:
- LINC00665通过miR-665/FGF9轴促进了软骨肉瘤的进展.
- 向LINC00665/miR-665/FGF9通路可能代表着一种新的治疗策略.
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