Background Gliomas are the most common malignant tumors of the central nervous system in adults, glioblastoma is notorious for its highly metastatic and recurrent, accounting for approximately 50% of all gliomas. Exploring its molecular mechanism is urgently needed for the treatment and prognosis evaluation of gliomas. Transmembrane BAX inhibitor motif-containing 1 (TMBIM1) has been reported to be associated with non-alcoholic steatohepatitis, tumor and other diseases. However, the role of TMBIM1 in GBM and the underlying mechanisms remains unclear.MethodsThe expression level and prognostic value of TMBIM1 in gliomas were investigated by public datasets, and further confirmed by western blot and immunohistochemistry (IHC) in our tissues. Intracranial xenograft model, IHC and western blot were used to evaluate the functional role of TMBIM1.ResultsTMBIM1 was over-expressed in GBM, and its high expression reduced the survival time of glioma patients. TMBIM1 induced EMT and autophagy, and inhibition of autophagy reverses TMBIM1-regulated EMT in vitro and in vivo. Intracranial xenograft model showed the survival time of mice in TMBIM1 knockdown group treated with chloroquine (CQ)was significantly prolonged. The loss of E-cadherin expression is considered the foundation of EMT, and we subsequently demonstrated that TMBIM1 stimulating autophagic degradation of E-cadherin via AMPK/mTOR/ULK1 axis. ConclusionOur study provides a novel mechanism for the regulation of EMT in the process of gliomas metastasis, indicating that inhibition of TMBIM1 activity to attenuate autophagy may be a potential strategy for the treatment of gliomas.