It has been recently discovered that the mitochondrial chaperone TRAP1 acts as a bona fide oncogene by down-modulating the activity of the respiratory complex II, aka succinate dehydrogenase. The consequent increase in intracellular succinate stabilizes the HIF1 transcription factor independently of oxygen availability, thus installing a pseudohypoxic phenotype that is instrumental in prompting tumor growth. It has been shown that TRAP1 takes part to complex regulatory networks that modulate mitochondrial metabolism, that include its interaction with F-ATP synthase. We aim at dissecting the mode(s) of regulation of tumor cell metabolism by TRAP1 interaction with F-ATP synthase and how this regulation affects tumor cell metabolism and viability, in order to identify novel approaches to selectively inhibit neoplastic growth
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