Abstract
Background and Aims : Normal hepatocytes in-vivo express only Sterol O-Acyltransferase2 (SOAT2), whereas in pathologic conditions (cancer) acquire SOAT1 expression. Hepatocytes mainly use mitochondrial oxidative metabolism for energy production, whereas cancer cells rely more on glycolysis for energy production. Currently, it is not known how cholesterol in mitochondria affects their metabolism, and whether SOAT2 and SOAT1 could play a role. Thus, we studied HepG2 cells and a unique cell model in which SOAT1 was genetically depleted: SOAT2-only-HepG2 cells.
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