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Evidence for Deficiency of Low Density Lipoprotein Receptor on Human Colonic Carcinoma Cell Lines¹

Departments of Microbiology [M. F., S. A. B.] and Pathology [S. A. B.], Boston University School of Medicine, Boston, Massachusetts 02118

Cells from six human colonic adenocarcinoma lines (CaCo-2, HT29, LS174T, SW480, SW403, and SW1417) and a normal skin fibroblast cell line (AG1519) were assayed in vitro for their ability to use low density lipoprotein (LDL). All tumor cell lines grew well in lipoprotein-deficient serum, implying that LDL in culture medium was not critical for cell growth. When cell growth was inhibited with mevinolin, a cholesterol synthesis inhibitor, the addition of LDL to the medium had no effect on the growth of cells from five of six tumor cell lines. CaCo-2 cells showed a moderate reversal while the fibroblast control showed total reversal of inhibition. A monoclonal antibody to bovine/human LDL receptor, used in an enzyme-linked immunosorbent assay, indicated that only CaCo-2 cells and human skin fibroblast cells consistently demonstrated the presence of LDL receptors. Thus, five of six colon tumor cell lines were unable to overcome a mevinolin block in cholesterol metabolism indicating that these cells were deficient in LDL receptors.

¹ This was supported in part by grant CA49227 and a training grant T-32-CA09423 from the National Cancer Institute, National Institutes of Health, and a Graduate Student Research Award from Boston University Division of Medical and Dental Sciences. Submitted in partial fulfillment of the requirements for the Doctor of Philosophy degree of the Division of Graduate Medical and Dental Sciences, Boston University School of Medicine.

² To whom requests for reprints should be addressed, at Department of Microbiology, Boston University School of Medicine, 80 East Concord Street, Boston, MA 02118.

Received 2/ 5/88. Revised 10/23/89. Accepted 10/27/89.

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