Malignant gliomas are a heterogeneous group of brain tumors with a poor prognosis, which is largely due to its aggressive invasiveness and angiogenesis. In recent years, it has been found that multiple long noncoding RNAs (lncRNAs) participate in a wide range of biological functions including angiogenesis through the regulation of gene expression in cancers. In this study, we investigate and report the novel role of lncRNA SLC26A4‐AS1 in gliomas, with a novel mechanism involving transcription factors NFKB1 and NPTX1. We determined that SLC26A4‐AS1 was downregulated in human glioma tissues and cells. Furthermore, overexpression of SLC26A4‐AS1 or NPTX1 restrained the aggressiveness of glioma cells and their pro‐angiogenic ability. SLC26A4‐AS1 was also found to upregulate NPTX1 by recruiting NFKB1 into the NPTX1 promoter. Moreover, silencing of either NPTX1 or NFKB1 restored the aggressive and pro‐angiogenic properties of glioma cells in the presence of SLC26A4‐AS1. Taken together, we demonstrate that SLC26A4‐AS1 promotes NPTX1 transcriptional activity by recruiting NFKB1 and thus exerting antiangiogenic effects on glioma cells. This study provides an experimental basis for the intervention of SLC26A4‐AS1 in the treatment of gliomas.