Endoplasmic Reticulum Stress in Gliomas: Exploiting a Dual-Effect Dysfunction through Chemical Pharmaceutical Compounds and Natural Derivatives for Therapeutical Uses

Author:

García-López Daniel12ORCID,Zaragoza-Ojeda Montserrat1ORCID,Eguía-Aguilar Pilar13ORCID,Arenas-Huertero Francisco14ORCID

Affiliation:

1. Laboratorio de Investigación en Patología Experimental, Hospital Infantil de México Federico Gómez, Mexico City 06720, Mexico

2. Facultad de Ciencia y Tecnología, Universidad Simón Bolívar, Mexico City 03920, Mexico

3. Departamento de Patología Clínica y Experimental, Hospital Infantil de México Federico Gómez, Mexico City 06720, Mexico

4. Centro de Investigación en Biomedicina y Bioseguridad, Hospital Infantil de México Federico Gómez, Mexico City 06720, Mexico

Abstract

The endoplasmic reticulum maintains proteostasis, which can be disrupted by oxidative stress, nutrient deprivation, hypoxia, lack of ATP, and toxicity caused by xenobiotic compounds, all of which can result in the accumulation of misfolded proteins. These stressors activate the unfolded protein response (UPR), which aims to restore proteostasis and avoid cell death. However, endoplasmic response-associated degradation (ERAD) is sometimes triggered to degrade the misfolded and unassembled proteins instead. If stress persists, cells activate three sensors: PERK, IRE-1, and ATF6. Glioma cells can use these sensors to remain unresponsive to chemotherapeutic treatments. In such cases, the activation of ATF4 via PERK and some proteins via IRE-1 can promote several types of cell death. The search for new antitumor compounds that can successfully and directly induce an endoplasmic reticulum stress response ranges from ligands to oxygen-dependent metabolic pathways in the cell capable of activating cell death pathways. Herein, we discuss the importance of the ER stress mechanism in glioma and likely therapeutic targets within the UPR pathway, as well as chemicals, pharmaceutical compounds, and natural derivatives of potential use against gliomas.

Funder

Fondos Federales Dirección de Investigación

Publisher

MDPI AG

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