Knockdown of USF1 Inhibits the Vasculogenic Mimicry of Glioma Cells via Stimulating SNHG16/miR-212-3p and linc00667/miR-429 Axis (Retracted article. See vol. 28, pg. 587, 2022)
Knockdown of USF1 Inhibits the Vasculogenic Mimicry of Glioma Cells via Stimulating SNHG16/miR-212-3p and linc00667/miR-429 Axis (Retracted article. See vol. 28, pg. 587, 2022)
复制标题
USF1 的敲低通过刺激 SNHG16/miR-212-3p 和 linc00667/miR-429 轴抑制神经胶质瘤细胞的血管生成拟态
DOI：
10.1016/j.omtn.2018.12.017
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发表时间：
2019-03-01
影响因子：
8.8
通讯作者：
Liu, Yunhui
中科院分区：
文献类型：
--
作者：
Wang, Di;Zheng, Jian;Liu, Yunhui
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对于改善患者总体中位生存期并不显着有效。因此，本研究探讨了神经胶质瘤中血管生成的模拟形成机制。本实验结果表明，胶质瘤组织和细胞中上游转录因子1（USF1）的表达上调。 USF1 敲低通过刺激 SNHG16 和 linc00667 抑制神经胶质瘤细胞中的增殖、迁移、侵袭、VM 和 VM 相关蛋白的表达。这两个长非编码 RNA (lncRNA) 通过影响神经胶质瘤 VM 的竞争性内源 RNA (ceRNA) 机制来调节 ALHD1A1。本研究首次证明USF1/SNHG16/miR-212-3p/ALDH1A1（乙醛脱氢酶-1）和USF1/linc00667/miR-429/ALDH1A1轴调节胶质瘤细胞的VM，这些发现可能为胶质瘤治疗提供新的策略。
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.