Glioblastoma multiforme (GBM) is the most malignant brain tumor with rapid angiogenesis. How to inhibit GBM angiogenesis is a key problem to be solved. To explore the targets of inhibiting GBM angiogenesis, this study confirmed that the expression of circMTA1 (hsa_circ_0033614) was significantly upregulated in human brain microvascular endothelial cells exposed to glioma cell‐conditioned medium (GECs). The expression of circMTA1 in the cytoplasm was significantly higher than that in the nucleus. Upregulated circMTA1 in GECs can promote cell proliferation, migration, and tube formation. Further exploration of the circularization mechanism of circMTA1 confirmed that KHDRBS1 protein can bind to the upstream and downstream flanking sequences of circMTA1 and promote circMTA1 biogenesis by coordinating Alu element pairing. KHDRBS1 upregulated the proliferation, migration, and tube formation of GECs by promoting the biogenesis of circMTA1. CircMTA1 can encode the protein MTA1‐134aa by internal ribosome entry site sequence‐mediated translation mechanism, and promote the proliferation, migration, and tube formation of GECs through the encoded MTA1‐134aa. This study provides a new target for inhibiting angiogenesis in brain GBM and a new strategy for improving the therapeutic efficacy of GBM. To explore the targets of inhibiting glioblastoma multiforme (GBM) angiogenesis, this study confirmed that circMTA1 was upregulated in human brain microvascular endothelial cells exposed in glioma cell‐conditioned medium (GECs). Mechanistic studies showed that KHDRBS1 cooperates with Alu elements in flanking introns of circMTA1 to promote circularization. CircMTA1 could translate into a 134aa protein termed MTA1‐134aa in an IRES‐dependent manner. MTA1‐134aa promoted GECs proliferation, migration, and tube formation. This study provides a new target for inhibiting angiogenesis in brain GBM.