Endoplasmic reticulum stress-induced cell death as a potential mechanism for targeted therapy in glioblastoma (Review)

Abstract

The endoplasmic reticulum (ER) is an essential organelle for protein synthesis, folding and modification, lipid synthesis, and calcium storage. When endogenous or exogenous stimuli lead to ER-synthesized protein folding dysfunction, numerous unfolded or misfolded proteins accumulate in the ER cavity and cause a series of subsequent responses, referred to as ER stress. If ER stress is continuous, the unfolded protein response (UPR) is not enough to remove the accumulated unfolded and misfolded proteins, and thus, UPR signaling pathways will drive cell apoptosis. Glioblastoma (GBM) is currently the most aggressive and common malignant tumor of the nervous system. Since ER stress may increase the sensitivity of GBM to temozolomide, this article reviews the possible mechanisms of ER stress-induced apoptosis and the factors affecting ER stress, and evaluates the potential of ER stress as a therapeutic target.