HIF1α-dependent uncoupling of glycolysis suppresses tumor cell proliferation

Hypoxia-inducible factor-1a (HIF1a) attenuates mitochondrial activity while promoting glycolysis. However, lower glycolysis is compromised in human clear cell renal cell carcinomas, in which HIF1a acts as a tumor suppressor by inhibiting cell-autonomous proliferation. Here, we find that, unexpectedl...

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Detalles Bibliográficos
Autores: Urrutia Elorduy, Andrés Amalio, Mesa Ciller, Claudia Julia, Guajardo Grence, Andrea, Alkan, H. Furkan, Soro Arnáiz, Inés, Vandekeere, Anke, Ferreira Campos, Ana Margarida, Igelmann, Sebastian, Fernández Arroyo Camacho, Lucía, Rinaldi, Gianmarco, Lorendeau, Doriane, Bock, Katrien De, Fendt, Sarah Maria, Aragonés López, Julián
Tipo de recurso: artículo
Fecha de publicación:2024
País:España
Institución:Universidad Autónoma de Madrid
Repositorio:Biblos-e Archivo. Repositorio Institucional de la UAM
Idioma:inglés
OAI Identifier:oai:repositorio.uam.es:10486/755080
Acceso en línea:https://hdl.handle.net/10486/755080
https://dx.doi.org/10.1016/j.celrep.2024.114103
Access Level:acceso abierto
Palabra clave:HIF1α
glycolysis
oxygen
renal cell carcinoma
mitochondria
NADH
hypoxia
tumor
Medicina
Descripción
Sumario:Hypoxia-inducible factor-1a (HIF1a) attenuates mitochondrial activity while promoting glycolysis. However, lower glycolysis is compromised in human clear cell renal cell carcinomas, in which HIF1a acts as a tumor suppressor by inhibiting cell-autonomous proliferation. Here, we find that, unexpectedly, HIF1a suppresses lower glycolysis after the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) step, leading to reduced lactate secretion in different tumor cell types when cells encounter a limited pyruvate supply such as that typically found in the tumor microenvironment in vivo. This is because HIF1a-dependent attenuation of mitochondrial oxygen consumption increases the NADH/NAD+ ratio that suppresses the activity of the NADHsensitive GAPDH glycolytic enzyme. This is manifested when pyruvate supply is limited, since pyruvate acts as an electron acceptor that prevents the increment of the NADH/NAD+ ratio. Furthermore, this antiglycolytic function provides a molecular basis to explain how HIF1a can suppress tumor cell proliferation by increasing the NADH/NAD+ ratio