METTL16介导的FGD5-AS1上调通过靶向miR-195-5p/SLC7A2轴促进骨肉瘤进展。
METTL16-Mediated Upregulation of FGD5-AS1 Promotes Progression of Osteosarcoma through Targeting of miR-195-5p/SLC7A2 Axis.
作者信息
Wu Weiqian, Zheng Wenbiao, Pan Weiwei, Chen Fanghu, Jiang Langqing
机构信息
Department of Orthopedics, Taizhou Municipal Hospital, Taizhou City, Zhejiang Province 318000, China.
Taizhou Municipal Hospital.
出版信息
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。
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