Wu Weiqian, Zheng Wenbiao, Pan Weiwei, Chen Fanghu, Jiang Langqing
Department of Orthopedics, Taizhou Municipal Hospital, Taizhou City, Zhejiang Province 318000, China.
Taizhou Municipal Hospital.
Crit Rev Eukaryot Gene Expr. 2025;35(5):17-31. doi: 10.1615/CritRevEukaryotGeneExpr.2025058118.
Dysregulated long noncoding RNAs (lncRNAs) promote the progression of osteosarcoma (OS). This study aimed to investigate the potential of lncRNA FGD5-AS1 in OS. Gene expression was determined using RT-qPCR. Protein expression was detected by western blot. N6-methyladenosine (m6A) modification was confirmed by MeRIP. Cell behaviors were detected using CCK-8, colony formation, and transwell assays. The interaction between miR-195-5p and the FGD5-AS1/SLC7A2 axis was confirmed by luciferase assays. FGD5-AS1 was upregulated in OS, induced by METTL16 via mediating m6A modification. However, FGD5-AS1 knockdown inhibited the proliferation and epithelial-mesenchymal transition (EMT) of OS cells. FGD5-AS1 sponged miR-195-5p to mediate the upregulation of SLC7A2, overexpression of which promoted aggressiveness of OS cells. In summary, METTL16-mediated upregulation of FGD5-AS1 promotes the aggressiveness of OS though targeting of miR-195-5p/SLC7A2 axis.
长链非编码RNA（lncRNA）失调促进骨肉瘤（OS）进展。本研究旨在探究lncRNA FGD5-AS1在骨肉瘤中的作用。采用RT-qPCR检测基因表达。通过蛋白质印迹法检测蛋白质表达。通过MeRIP法确认N6-甲基腺苷（m6A）修饰。使用CCK-8、集落形成和Transwell实验检测细胞行为。通过荧光素酶实验确认miR-195-5p与FGD5-AS1/SLC7A2轴之间的相互作用。FGD5-AS1在骨肉瘤中上调，由METTL16通过介导m6A修饰诱导产生。然而，敲低FGD5-AS1可抑制骨肉瘤细胞的增殖和上皮-间质转化（EMT）。FGD5-AS1吸附miR-195-5p以介导SLC7A2的上调，SLC7A2的过表达促进骨肉瘤细胞的侵袭性。总之，METTL16介导的FGD5-AS1上调通过靶向miR-195-5p/SLC7A2轴促进骨肉瘤的侵袭性。
