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Background Mechanisms involved in regulating metabolic reprogramming in cancer cells are not fully understood. Acetylation is emerging as a major regulator of mitochondrial metabolism and may contribute to metabolic derangements that occur in cancer cells. Sirtuin-3, (SIRT3), is the main mitochondrial deacetylase and it serves to maintain mitochondrial energy homeostasis by deacetylating and activating mitochondrial proteins. Loss of SIRT3 leads to altered cellular metabolism including reduced ATP production and decreased fatty acid oxidation [1]. Remarkably, reduced SIRT3 expression is associated with cancer in patients and Sirt3 knockout mice [2]. However, the mechanism of mitochondrial protein hyperacetylation and the sub-sequent increased susceptibility to tumor formation remains unknown.

Loss of SIRT3 leads to a compensatory shift in cellular metabolism promoting cancer cell growth