Abstract
The mitochondrial ATP synthase is a multi-subunit enzyme complex located in the inner mitochondrial membrane which is essential for oxidative phosphorylation under physiological conditions. In this review, we analyse the enzyme functions involved in cancer progression by dissecting specific conditions in which ATP synthase contributes to cancer development or metastasis. Moreover, we propose the role of ATP synthase in the formation of the permeability transition pore (PTP) as an additional mechanism which controls tumour cell death. We further describe transcriptional and translational modifications of the enzyme subunits and of the inhibitor protein IF1 that may promote adaptations leading to cancer metabolism. Finally, we outline ATP synthase gene mutations and epigenetic modifications associated with cancer development or drug resistance, with the aim of highlighting this enzyme complex as a potential novel target for future anti-cancer therapy.
Highlights
Cancer cells undergo alterations in metabolic pathways that enable a number of regulatory processes, such as the enlargement of biosynthetic precursor pools, the production of signalling molecules or the generation of metabolites for post-translational or epigeneticThe rate of oxidative phosphorylation is regulated by the activity of the mitochondrial ATP synthase (Boyer 1997)
We analyse the enzyme functions involved in cancer progression by dissecting specific conditions in which ATP synthase contributes to cancer development or metastasis
Mitochondria participate to the metabolic and biosynthetic pathways that drive cancer development and progression
Summary
Cancer cells undergo alterations in metabolic pathways that enable a number of regulatory processes, such as the enlargement of biosynthetic precursor pools, the production of signalling molecules or the generation of metabolites for post-translational or epigeneticThe rate of oxidative phosphorylation is regulated by the activity of the mitochondrial ATP synthase (Boyer 1997). We list several mutations, transcriptional changes or epigenetic modifications at the ATP synthase gene level, that are responsible for the metabolic rewiring during cancer development or are associated to drug resistance.
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