Acetate Induces Growth Arrest in Colon Cancer Cells Through Modulation of Mitochondrial Function

Acetate is one of the main short chain fatty acids produced in colon when fermentable carbohydrates are digested. It has been shown to affect normal metabolism, modulating mitochondrial function, and acid oxidation. Currently, there no clear consensus regarding effects acetate on tumorigenesis cancer metabolism. Here, we investigate metabolic cancer. HT29 HCT116 cell lines were treated with its effect proliferation, reactive oxygen species, density, permeability transition pore, cellular bioenergetics, gene expression acetyl-CoA synthetase 1 ( ACSS1 ) 2 ACSS2 ), lipid levels investigated. was found reduce proliferation both under normoxia as well reducing glycolysis; it also increase consumption ROS levels. Cell death observed independent ACSS1/2 expression. Under hypoxic conditions, reduced maintained line but longer line. together increased hypoxia which may partly protect cells from anti-proliferative reversed Warburg caused by acetate. The findings this study suggest that a consequence impact metabolism during ACCS1/2