The role of endoplasmic reticulum stress in promoting aerobic glycolysis in cancer cells: An overview.

Autor: Jalil AT; College of Medicine, University of Thi-Qar, Al-Nasiriyah, Thi-Qar, Iraq. Electronic address: abedalazeem799@gmail.com., Abdulhadi MA; Department of Medical Laboratory Techniques, Al-Maarif University College, Al-Anbar, Iraq., Alkubaisy SA; Desert Studies Center, Al-Anbar University, Al-Anbar, Iraq., Thejeel SH; National University of Science and Technology, Al-Nasiriyah, Thi-Qar, Iraq., Essa IM; Department of Veterinary Parasitology, College of Veterinary Medicine, University of Basrah, Basrah, Iraq., Merza MS; Prosthetic Dental Techniques Department, Al-Mustaqbal, University College, Hillah, Babylon, Iraq., Zabibah RS; Medical Laboratory Technology Department, College of Medical Technology, The Islamic University of Najaf, Najaf, Iraq., Al-Tamimi R; Medical Technical College, Al-Farahidi University, Baghdad, Iraq.
Jazyk: angličtina
Zdroj: Pathology, research and practice [Pathol Res Pract] 2023 Nov; Vol. 251, pp. 154905. Date of Electronic Publication: 2023 Oct 24.
DOI: 10.1016/j.prp.2023.154905
Abstrakt: Aerobic glycolysis, also known as the Warburg effect, is a metabolic phenomenon frequently observed in cancer cells, characterized by the preferential utilization of glucose through glycolysis, even under normal oxygen conditions. This metabolic shift provides cancer cells with a proliferative advantage and supports their survival and growth. While the Warburg effect has been extensively studied, the underlying mechanisms driving this metabolic adaptation in cancer cells remain incompletely understood. In recent years, emerging evidence has suggested a potential link between endoplasmic reticulum (ER) stress and the promotion of aerobic glycolysis in cancer cells. The ER is a vital organelle involved in protein folding, calcium homeostasis, and lipid synthesis. Various cellular stresses, such as hypoxia, nutrient deprivation, and accumulation of misfolded proteins, can lead to ER stress. In response, cells activate the unfolded protein response (UPR) to restore ER homeostasis. However, prolonged or severe ER stress can activate alternative signaling pathways that modulate cellular metabolism, including the promotion of aerobic glycolysis. This review aims to provide an overview of the current understanding regarding the influence of ER stress on aerobic glycolysis in cancer cells to shed light on the complex interplay between ER stress and metabolic alterations in cancer cells. Understanding the intricate relationship between ER stress and the promotion of aerobic glycolysis in cancer cells may provide valuable insights for developing novel therapeutic strategies targeting metabolic vulnerabilities in cancer.
Competing Interests: Declaration of Competing Interest We would like to submit a review article entitled “The Role of Endoplasmic Reticulum Stress in Promoting Aerobic Glycolysis in Cancer Cells: An Overview” by Abduladheem Turki Jalil, Mohanad Ali Abdulhadi, Sami Awad Alkubaisy, Sara Hamed Thejeel, Israa M. Essa, Muna S. Merza, Rahman S. Zabibah, Raad Al-Tamimi for possible publication in Pathology – Research and Practice; and the authors declare that they have no conflict of interest.
(Copyright © 2023 Elsevier GmbH. All rights reserved.)
Databáze: MEDLINE
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