SNAI2 and glioma: For example, FoxM1 potentiates WNT pathway activation by facilitating β-catenin nuclear accumulation and direct transcriptional upregulation of WNT pathway target genes.[13, 32] Other reports have shown that FoxM1 binds to VEGF promoter and regulates VEGF expression in glioma cells.[33, 34] In pancreatic cancer, FoxM1 stimulates epithelial-mesenchymal transition (EMT), invasion and angiogenesis.[35] In breast cancer, FoxM1 promotes EMT by regulating Slug expression and its knockdown inhibits mesenchymal phenotype.[36] Here, we showed that FoxM1 induces transcription of Sox2 in GBM cells.