血管生成
胶质瘤
基因敲除
下调和上调
癌症研究
信使核糖核酸
化学
生物
细胞生物学
转移
癌症
细胞培养
生物化学
遗传学
基因
作者
Angelo Pan,Yixue Xue,Xuelei Ruan,Wei Dong,Di Wang,Yunhui Liu,Libo Liu,Yang Liu,E Tiange,Hongda Lin,Haidong Xu,Xiaobai Liu,Ping Wang
标识
DOI:10.1016/j.ijbiomac.2023.128409
摘要
Angiogenesis plays a major role in tumor initiation, progression, and metastasis. This is why finding antiangiogenic targets is essential in the treatment of gliomas. In this study, NSUN2 and LINC00324 were significantly upregulated in conditionally cultured glioblastoma endothelial cells (GECs). Knockdown of NSUN2 or LINC00324 inhibits GECs angiogenesis. NSUN2 increased the stability of LINC00324 by m5C modification and upregulated LINC00324 expression. LINC00324 competes with the 3’UTR of CBX3 mRNA to bind to AUH protein, reducing the degradation of CBX3 mRNA. In addition, CBX3 directly binds to the promoter region of VEGFR2, enhances VEGFR2 transcription, and promotes GECs angiogenesis. These findings demonstrated NSUN2/LINC00324/CBX3 axis plays a crucial role in regulating glioma angiogenesis, which provides new strategies for glioma therapy.
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