Alteration of glucose metabolism and expression of glucose transporters in ovarian cancer

Author:

Ben Ali Fatima1,Qmichou Zineb2,Oukabli Mohamed3,Dakka Nadia1,Bakri Youssef1,Eddouks Mohammed4,Ameziane El Hassani Rabii1

Affiliation:

1. Laboratory of Biology of Human Pathologies (BioPatH), Faculty of Sciences, Mohammed V University in Rabat, Rabat 10001, Morocco

2. Medical Biotechnology Center, Moroccan Foundation for Advanced Science, Innovation and Research (MAScIR), Rabat 10001, Morocco

3. Department of Anatomical Pathology, Military Hospital of Instruction Mohammed V (HMIMV-R), Faculty of Medicine and Pharmacy, Mohammed V University in Rabat, Rabat 10001, Morocco

4. Team of Ethnopharmacology and Pharmacognosy, Faculty of Sciences and Techniques Errachidia, Moulay Ismail University of Meknes, Errachidia BP 509, Morocco

Abstract

Aerobic glycolysis also known as the Warburg effect, remains a hallmark of various cancers, including ovarian cancer. Cancer cells undergo metabolic changes to sustain their tumorigenic properties and adapt to environmental conditions, such as hypoxia and nutrient starvation. Altered metabolic pathways not only facilitate ovarian cancer cells’ survival and proliferation but also endow them to metastasize, develop resistance to chemotherapy, maintain cancer stem cell phenotype, and escape anti-tumor immune responses. Glucose transporters (GLUTs), which play a pivotal role as the rate-limiting step in glycolysis, are frequently overexpressed in a variety of tumors, including ovarian cancer. Multiple oncoproteins can regulate GLUT proteins, promoting tumor proliferation, migration, and metastasis, either dependent or independent of glycolysis. This review examines the alteration of GLUT proteins, particularly GLUT1, in ovarian cancer and its impact on cancer initiation, progression, and resistance to treatment. Additionally, it highlights the role of these proteins as biomarkers for diagnosis and prognosis in ovarian cancer, and delves into novel therapeutic strategies currently under development that target GLUT isoforms.

Publisher

Open Exploration Publishing

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