Antiangiogenic
therapy plays a significant role in combined
glioma treatment. However, poor permeability of the blood-
tumor barrier (BTB) limits the transport of chemotherapeutic agents, including antiangiogenic drugs, into
tumor tissues. Long non-coding RNAs (lncRNAs) have been implicated in various diseases, especially malignant
tumors. The present study found that
lncRNA X-inactive-specific transcript (XIST) was upregulated in endothelial cells that were obtained in a BTB model in vitro. XIST knockdown increased BTB permeability and inhibited
glioma angiogenesis. The analysis of the mechanism of action revealed that the reduction of XIST inhibited the expression of the
transcription factor forkhead box C1 (FOXC1) and zonula occludens 2 (ZO-2) by upregulating miR-137. FOXC1 decreased BTB permeability by increasing the promoter activity and expression of ZO-1 and
occludin, and promoted
glioma angiogenesis by increasing the promoter activity and expression of
chemokine (C-X-C motif) receptor 7b (CXCR7). Overall, the present study demonstrates that XIST plays a pivotal role in BTB permeability and
glioma angiogenesis, and the inhibition of XIST may be a potential target for the clinical management of
glioma.