Energy metabolism transition in multi-cellular human tumor spheroids


Por: Rodríguez-Enríquez S., Gallardo-Pérez J.C., Avilés-Salas A., Marín-Hernández A., Carreño-Fuentes L., Maldonado-Lagunas V., Moreno-Sánchez R.

Publicada: 1 ene 2008
Resumen:
It is thought that glycolysis is the predominant energy pathway in cancer, particularly in solid and poorly vascularized tumors where hypoxic regions develop. To evaluate whether glycolysis does effectively predominate for ATP supply and to identify the underlying biochemical mechanisms, the glycolytic and oxidative phosphorylation (OxPhos) fluxes, ATP/ADP ratio, phosphorylation potential, and expression and activity of relevant energy metabolism enzymes were determined in multi-cellular tumor spheroids, as a model of human solid tumors. In HeLa and Hek293 young-spheroids, the OxPhos flux and cytochrome c oxidase protein content and activity were similar to those observed in monolayer cultured cells, whereas the glycolytic flux increased two- to fourfold; the contribution of OxPhos to ATP supply was 60%. In contrast, in old-spheroids, OxPhos, ATP content, ATP/ADP ratio, and phosphorylation potential diminished 50-70%, as well as the activity (88%) and content (3 times) of cytochrome c oxidase. Glycolysis and hexokinase increased significantly (both, 4 times); consequently glycolysis was the predominant pathway for ATP supply (80%). These changes were associated with an increase (3.3 times) in the HIF-1a content. After chronic exposure, both oxidative and glycolytic inhibitors blocked spheroid growth, although the glycolytic inhibitors, 2-deoxyglucose and gossypol (IC50 of 15-17 nM), were more potent than the mitochondrial inhibitors, casiopeina II-gly, laherradurin, and rhodamine 123 (IC50 > 100 nM). These results suggest that glycolysis and OxPhos might be considered as metabolic targets to diminish cellular proliferation in poorly vascularized, hypoxic solid tumors. © 2008 Wiley-Liss, Inc.

Filiaciones:
Rodríguez-Enríquez S.:
 Departamento de Bioquímica, Instituto Nacional de Cardiología, Mexico, Mexico

 Departamento de Bioquimica, Instituto Nacional de Cardiologia, Juan Badiano No. 1, Tlalpan, Mexico D F 14080, Mexico

Gallardo-Pérez J.C.:
 Departamento de Bioquímica, Instituto Nacional de Cardiología, Mexico, Mexico

Avilés-Salas A.:
 Departamentos de Biología Molecular Y de Paralogía, Instituto Nacional de Cancerología, Mexico, Mexico

Marín-Hernández A.:
 Departamento de Bioquímica, Instituto Nacional de Cardiología, Mexico, Mexico

Carreño-Fuentes L.:
 Departamento de Bioquímica, Instituto Nacional de Cardiología, Mexico, Mexico

Maldonado-Lagunas V.:
 Departamentos de Biología Molecular Y de Paralogía, Instituto Nacional de Cancerología, Mexico, Mexico

Moreno-Sánchez R.:
 Departamento de Bioquímica, Instituto Nacional de Cardiología, Mexico, Mexico
ISSN: 00219541
Editorial
Wiley-Liss Inc., DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 216 Número: 1
Páginas: 189-197
WOS Id: 000256600800022
ID de PubMed: 18264981

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