MET and glioblastoma: Hei et al. demonstrated in vitro (U87 and U251 cells) and in a U87-luciferase orthotopic xenograft mouse model that ACT inhibits GBM cell growth, reduces the receptor tyrosine kinase (c-Met) and epithelial-to-mesenchymal transition (EMT) marker levels (snail, vimentin, zeb1), and exerts antitumor effects by directly targeting c-Met, leading to its degradation via the ubiquitination–proteasome pathway [66].