Background
Fatty acids from conjugated linoleic acid (CLA)-enriched egg yolk suppressed the viability of the MCF-7 cancer line more effectively than non-enriched egg yolk. Herein we aimed to determine the molecular mechanisms by analysing the expression and activation of proteins involved in cellular stress and apoptosis signaling. Materials and
Conclusion
Taken together, our results suggest that activation of the mitochondrial apoptotic pathway may be a potential mechanism of EFA-CLA action.
Methods
Forty-eight Isa Brown laying hens (26-week-old) were fed a fortified (0.75% CLA) or a control diet (0% CLA) for 4 months. Collected eggs were used to obtain CLA-enriched (EFA-CLA) or non-enriched (EFA) fatty acid extracts for the treatment of the MCF-7 cancer cell line. Protein levels were analysed by PathScan® Stress and Apoptosis Signalling Antibody Array and western blot method.
Results
Treatment with EFA-CLA led to activation of caspase signalling as main effector of apoptosis. It also increased levels of pro-apoptotic B-cell lymphoma 2 family proteins as well as promoted the release of cytochrome c, second mitochondria-derived activator of caspase and mitochondrial serine protease from mitochondria to the cytoplasm. EFA-CLA increased levels of tumour protein 53 and mothers against decapentaplegic homolog 2 tumour suppressors, and activated p38 mitogen-activated protein kinases and stress-activated protein kinase/c-Jun NH2-terminal kinase proteins. Finally, treatment down-regulated anti-apoptotic extracellular signal-regulated protein kinases 1 and 2, RAC-alpha serine/threonine-protein kinase, heat-shock protein 27, inhibitor of nuclear factor κβ, transforming growth factor beta-activated kinase 1 and survivin proteins.