The anti-angiogenic treatment of malignant glioma cells is an effective method to treat high-grade gliomas. However, due to the presence of vasculogenic mimicry (VM), the anti-angiogenic treatment of gliomas is not significantly effective in improving overall patient median survival. Therefore, this study investigated the mechanism of mimic formation of angiogenesis in gliomas. The results of this experiment indicate that the expression of upstream transcription factor 1 (USF1) is upregulated in glioma tissues and cells. USF1 knockdown inhibits the proliferation, migration, invasion, VM, and expression of VM-associated proteins in glioma cells by stimulating SNHG16 and linc00667. These two long non-coding RNAs (lncRNAs) regulate ALHD1A1 through the competing endogenous RNA (ceRNA) mechanism influencing the VM of glioma. This study is the first to demonstrate that the USF1/SNHG16/miR-212-3p/ALDH1A1 (aldehyde dehydrogenase-1) and USF1/linc00667/miR-429/ALDH1A1 axis regulates the VM of glioma cells, and these findings might provide a novel strategy for glioma treatment.

恶性胶质瘤细胞的抗血管生成治疗是治疗高级别胶质瘤的有效方法。然而，由于血管生成拟态（VM）的存在，神经胶质瘤的抗血管生成治疗在提高患者的总体中位生存率方面并不显着有效。因此，本研究探讨了胶质瘤中模拟血管生成的机制。该实验的结果表明上游转录因子1（USF1）的表达在胶质瘤组织和细胞中上调。USF1 敲低通过刺激 SNHG16 和 linc00667 抑制胶质瘤细胞中 VM 相关蛋白的增殖、迁移、侵袭、VM 和表达。这两种长链非编码 RNA (lncRNA) 通过影响胶质瘤 VM 的竞争性内源性 RNA (ceRNA) 机制调节 ALHD1A1。