Alteration of the bioenergetic phenotype of mitochondria is a hallmark of breast, gastric, lung and oesophageal cancer

• Published in: Biochemical journal Vol. 378; no. Pt 1; pp. 17 - 20
• Main Authors: Isidoro, Antonio, Martínez, Marta, Fernández, Pedro L, Ortega, Alvaro D, Santamaría, Gema, Chamorro, Margarita, Reed, John C, Cuezva, José M
• Format: Journal Article
• Language: English
• Published: England 15.02.2004
• Subjects: Adenocarcinoma - metabolism; Breast Neoplasms - metabolism; Carcinoma - metabolism; Carcinoma, Squamous Cell - metabolism; Chaperonin 60 - metabolism; Energy Metabolism; Esophageal Neoplasms - metabolism; Female; Glycolysis; Humans; Lung Neoplasms - metabolism; Male; Mitochondria - metabolism; Oxidative Phosphorylation; Phenotype; Prostatic Neoplasms - metabolism; Proton-Translocating ATPases - metabolism; Stomach Neoplasms - metabolism
• ISSN: 0264-6021; 1470-8728
• DOI: 10.1042/bj20031541

Recent findings indicate that the expression of the beta-catalytic subunit of the mitochondrial H+-ATP synthase (beta-F1-ATPase) is depressed in liver, kidney and colon carcinomas, providing further a bioenergetic signature of cancer that is associated with patient survival. In the present study, we performed an analysis of mitochondrial and glycolytic protein markers in breast, gastric and prostate adenocarcinomas, and in squamous oesophageal and lung carcinomas. The expression of mitochondrial and glycolytic markers varied significantly in these carcinomas, when compared with paired normal tissues, with the exception of prostate cancer. Overall, the relative expression of beta-F1-ATPase was significantly reduced in breast and gastric adenocarcinomas, as well as in squamous oesophageal and lung carcinomas, strongly suggesting that alteration of the bioenergetic function of mitochondria is a hallmark of these types of cancer.