Effects of low‐ and high‐density lipoproteins on the proliferation of human breast cancer cells In vitro: Differences between hormone‐dependent and hormone‐independent cell lines

Abstract

The influence of low- and high-density lipoproteins on the proliferation of human breast cancer cells in culture was studied. We compared total cell number after incubation for 48 hr in culture medium containing or lacking plasma lipoproteins. Marked differences were found between hormone-dependent (MCF-7, T-47-D, ZR-75) and hormone-independent (MDA-MB-231, HBL-100) mammary tumor cell lines. The cells also reacted differently on the different lipoproteins offered in the medium. Human low-density lipoproteins (LDL) exhibited a marked stimulation of the growth of hormone-independent cell lines but no or only toxic effects upon the hormone-sensitive lines. Human high-density lipoproteins (HDL) stimulated the proliferation of all cell lines in a dose-dependent manner but hormone-independent cells showed a higher response. These findings point towards different utilizations of nutrients in hormone-dependent and hormone-independent cells.

Metabolic syndrome affects breast cancer risk in postmenopausal women: National Cancer Institute of Naples experience

“…25 In vitro studies have shown that low serum HDL-C stimulates the growth of hormone dependent breast cancer cells. 23,24,26 Low serum HDL-C is independently associated with increased postmenopausal breast cancer risk among obese and overweight women. Furthermore serum HDL-C may be considered a marker of androgen status, because hormones finely tune the levels of serum HDL-C, by regulating the activity of the lipolytic enzyme hepatic lipase.…”

Lipoproteins and Cancer

“…Although the mechanism was not clear, the data implied that HDL as well as LDL could be a source of CE for leukemic cells. A previous study in BrC cells showed that either HDL or LDL dose-dependently stimulated proliferation of ER-cell lines, but only HDL had the effect on ER+ cells lines (Rotheneder and Kostner 1989). In an animal model of PrC, a diet high in fat and cholesterol resulted in increased tumor incidence and increased tumor expression of scavenger receptor B1, the receptor responsible for selective uptake of HDL-C (the major form of circulating cholesterol in mice) by cells (Llaverias, Danilo et al 2010).…”

The human breast carcinoma cell line HBL-100 acquires exogenous cholesterol from high-density lipoprotein via CLA-1 (CD-36 and LIMPII analogous 1)-mediated selective cholesteryl ester uptake

“…pronounced for oestrogen-receptor-positive cells as compared with oestrogen-receptor-negative cell lines [5].…”