Autophagy is a process essential for cellular energy consumption, survival, and defense mechanisms. The role of autophagy in several types of human cancers has been explicitly explained; however, the underlying molecular mechanism of autophagy in glioblastoma remains ambiguous. Autophagy is thought to be a “double-edged sword”, and its effect on tumorigenesis varies with cell type. On the other hand, autophagy may play a significant role in the resistance mechanisms against various therapies. Therefore, it is of the utmost importance to gain insight into the molecular mechanisms deriving the autophagy-mediated therapeutic resistance and designing improved treatment strategies for glioblastoma. In this review, we discuss autophagy mechanisms, specifically its pro-survival and growth-suppressing mechanisms in glioblastomas. In addition, we try to shed some light on the autophagy-mediated activation of the cellular mechanisms supporting radioresistance and chemoresistance in glioblastoma. This review also highlights autophagy’s involvement in glioma stem cell behavior, underlining its role as a potential molecular target for therapeutic interventions.

A 28-year-old woman presented with a rare primary epidural hemangioma without adjacent vertebral involvement manifesting as progressive paraparesis. Magnetic resonance imaging of the thoracic spine showed an epidural lesion at T4-5 space appearing as isointense on T1-weighted images with enhancement by contrast medium and hyperintense on T2-weighted images. The lesion was totally removed microsurgically. Histological examination revealed cavernous hemangioma. She made a complete recovery from her symptoms and has remained asymptomatic for 9 years.