Fig. 1

Overview of cholesterol homeostasis pathways utilized in cancer. Cells obtain cholesterol by taking it up from the extracellular environment or by de novo synthesis. Excess intracellular cholesterol can be transported out of cells with specific efflux mechanisms including ATP-binding cassette (ABC) transporters ABCA1 and ABCG1. Cholesterol uptake involves receptor mediated endocytosis, macropinocytosis and the cooperation of lysosomes resulting in a release of the free cholesterol from cholesteryl ester. The cholesterol levels will affect the regulatory machinery, low cholesterol levels lead to increase transcription through SREBP-2 activation and high cholesterol levels leads to the deactivation of SREBP-2, activation of LXR and the storage of cholesteryl esters in lipid droplets. ABCA1 (ATP-binding cassette transporter A1), ABCG1 (ATP Binding Cassette Subfamily G Member 1), HDL (high density lipoprotein), LDL (low density lipoprotein), LDLR (Low density lipoprotein receptor) LXR (Liver X receptor), NPC1 and NPC2 (Niemann-Pick type C protein 1 and 2), HMGCR (HMG-CoA reductase), SR-B1 (Scavenger receptor class B type 1), SREBP-2 (Sterol regulatory element-binding protein 2), SCAP (SREBP-2 cleavage activation protein), INSIG (Insulin-induced gene protein)