Acetate is a driver of quiescence in ovarian cancer

While prior work in muscle cells indicates that metabolic reprogramming is associated with quiescence, whether metabolic changes occur in cancer to drive quiescence is unclear. Using a multi-omics approach, we found that the metabolic enzyme ACSS2 is both highly upregulated in quiescent cells and required for their survival. ACSS2 converts acetate into acetyl-CoA, and we confirmed increased acetate-derived acetyl-CoA in quiescent cells, demonstrating increased ACSS2 activity. Interestingly, supplementing cells with acetate alone was sufficient to induce a reversible quiescent cell cycle exit. We treated Ovcar8 high grade serous cancer cells with 10mM sodium acetate for 72h. Controls were untreated. All samples were done in triplicate. Comparative gene expression profiling analysis for control and acetate-treated Ovcar8 cells.