Autophagic-Related Proteins in Brain Gliomas: Role, Mechanisms, and Targeting Agents

Abstract

The present review focuses on the phenomenon of autophagy, a catabolic cellular process, which allows for the recycling of damaged organelles, macromolecules, and misfolded proteins. The different steps able to activate autophagy start with the formation of the autophagosome, mainly controlled by the action of several autophagy-related proteins. It is remarkable that autophagy may exert a double role as a tumour promoter and a tumour suppressor. Herein, we analyse the molecular mechanisms as well as the regulatory pathways of autophagy, mainly addressing their involvement in human astrocytic neoplasms. Moreover, the relationships between autophagy, the tumour immune microenvironment, and glioma stem cells are discussed. Finally, an excursus concerning autophagy-targeting agents is included in the present review in order to obtain additional information for the better treatment and management of therapy-resistant patients.

The Role of Autophagy in Brain Tumors

“…Novel methods such as clustered regularly interspaced short palindromic repeats (CRISPRs)-CRISPR-associated protein (Cas9) genome editing and/or application of miRNAs and high-throughput technologies are underlined as key technologies to identify and understand autophagy targets in gliomas, in order to obtain additional information for the better treatment and management of therapy-resistant patients. Thus, it is suggested that this modern perspective could help in the selection of patients with gliomas that are most likely to respond to autophagy inhibition therapy, but also to identify patients resistant to treatment [6].…”