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

Milk enriched in conjugated linoleic acid (CLA) was obtained from cows on pasture supplemented with full-fat rapeseeds (FFR; 2·26 g cis 9, trans 11 (c9, t11)-CLA/100 g fatty acid methyl esters) and full-fat soyabeans (1·83 g c9, t11-CLA/100 g fatty acid methyl esters). A control milk fat (1·69 g c9, t11-CLA/100 g 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 c9, t11-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 4 d with milk fats (yielding CLA concentrations between 60·2 and 80·6 (mu)M). The FFR milk fat, containing the highest CLA content, increased (P<0· 05) [14C]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) [14C]AA conversion to prostaglandin (PG) E2 while increasing conversion to PGF2(alpha) in both cell lines. All milk-fat samples increased (P<0·05) lipid peroxidation as measured by 8-epi-PGF2(alpha) 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.