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 no... More
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.
