Low density lipoprotein-receptor activity is lost in vivo in malignantly transformed renal tissue.
Mammalian cells can acquire cholesterol through two tightly regulated pathways, namely de novo cholesterol synthesis and receptor-mediated endocytosis of circulating low density lipoprotein (LDL). Malignant cells growing in vitro acquire cholesterol through both mechanisms but the quantitative importance of these pathways to a cancer growing in vivo is not known. Using the Lewis rat renal carcinoma model, this study measured the rate of cholesterol acquisition via both pathways in vivo in both normal and malignant renal tissue. In contrast to normal kidney, after malignant transformation, LDL-receptor activity disappeared entirely and the cancer acquired the cholesterol needed for growth by a 5-fold increase in the rate of cholesterol synthesis.
D000230:Adenocarcinoma / Q000378:metabolism*; D000818:Animals; D001692:Biological Transport; D002784:Cholesterol / Q000096:biosynthesis*; D007680:Kidney Neoplasms / Q000378:metabolism*; D008077:Lipoproteins, LDL / Q000378:metabolism*; D051381:Rats; D011917:Rats, Inbred Lew; D011973:Receptors, LDL / Q000032:analysis*
D008077:Lipoproteins, LDL; D011973:Receptors, LDL; D002784:Cholesterol