The Relevance of the Mitochondrial H+-ATP Synthase in Cancer Biology

摘要: Cancer cells depend on metabolic changes to cover the increased energy and metabolite demands that sustain proliferation. The enhanced rate of aerobic glycolysis activation other pathways provide building blocks support cell division. These occurred in response partial silencing bioenergetic function mitochondria, specifically H+-ATP synthase, which is engine produces most ATP sustains cellular activities normal differentiated cells. Changes phenotype carcinomas can be assessed by determination expression catalytic subunit synthase (β-F1-ATPase) relative enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH). β-F1-ATPase/GAPDH ratio provides a signature tumor with clinical relevance as molecular marker prognosis different cancer patients well chemotherapy. Energy metabolism has become an attractive target for therapy because it common phenotypic trait carcinomas. In addition, prevalent also exerted at activity level overexpression ATPase inhibitory factor 1 (IF1), protein contributes rewiring signaling death-resistant phenotypes