We showed that (1) THBS1 expression is greater in high-grade glioma patients samples when compared with low-grade gliomas; (2) THBS1 expression is regulated by TGFβ1 via SMAD3-binding sites; (3)THBS1 is both expressed in tumour cells and vessels; (4) tumour-derived THBS1 is involved in GBM invasion and expansion; (5) anti-angiogenic treatment increases THBS1 expression through hypoxia-induced TGFβ1; (6) tumour cell-bound CD47 is involved in THBS1 effects; (7) network analysis demonstrates THBS1 as the gene with the highest connectivity in the invasive compartment. Here, SMAD3 is linked to neoplasm.