Conjugated linoleic acid (CLA)-enriched milk fat inhibits growth and modulates CLA-responsive biomarkers in MCF-7 and SW480 human cancer cell lines

Abstract

Milk enriched in conjugated linoleic acid (CLA) was obtained from cows on pasture supplemented with full-fat rapeseeds (FFR; 2·26g cis 9, trans 11 ( c 9, t 11)-CLA/100g fatty acid methyl esters) and full-fat soyabeans (1·83g c 9, t 11-CLA/100g fatty acid methyl esters). A control milk fat (1·69g c 9, t 11-CLA/100g fatty acid methyl esters) was obtained from cows fed on pasture only. The present study assessed the potency of the CLA-enriched milk fats to modulate biomarkers that had previously been observed to respond to c 9, t 11-CLA in the MCF-7 and SW480 cell lines. Cell numbers decreased ( P <0·05) by up to 61 and 58% following the incubation of MCF-7 and SW480 cells, respectively, for 4d with milk fats (yielding CLA concentrations between 60·2 and 80·6μM). The FFR milk fat, containing the highest CLA content, increased ( P <0·05) [ 14 C]arachidonic acid (AA) uptake into the monoacylglycerol fraction of MCF-7 and SW480 cells while it decreased ( P <0·05) uptake into the phospholipid fraction of the latter. This milk fat also decreased ( P <0·05) [ 14 C]AA conversion to prostaglandin (PG) E 2 while increasing conversion to PGF 2 α in both cell lines. All milk-fat samples increased ( P <0·05) lipid peroxidation as measured by 8-epi-PGF 2 α in both cell lines. In SW480 cells the milk-fat samples decreased ( P <0·05) bcl-2 and cytosolic glutathione levels while increasing ( P <0·05) membrane-associated annexin V levels. All milk-fat samples decreased ( P <0·05) the expression of ras in SW480 cells. These data suggest that milk-fat CLA was effective at modulating synthetic CLA-responsive biomarkers.