Fatty Acids of CLA-Enriched Egg Yolks Can Induce Transcriptional Activation of Peroxisome Proliferator-Activated Receptors in MCF-7 Breast Cancer Cells

Aneta A Koronowicz; Paula Banks; Adam Master; Dominik Domagała; Ewelina Piasna-Słupecka; Mariola Drozdowska; Elżbieta Sikora; Piotr Laidler

doi:10.1155/2017/2865283

Fatty Acids of CLA-Enriched Egg Yolks Can Induce Transcriptional Activation of Peroxisome Proliferator-Activated Receptors in MCF-7 Breast Cancer Cells

PPAR Res. 2017:2017:2865283. doi: 10.1155/2017/2865283. Epub 2017 Mar 26.

Authors

Aneta A Koronowicz¹, Paula Banks¹, Adam Master², Dominik Domagała¹, Ewelina Piasna-Słupecka¹, Mariola Drozdowska¹, Elżbieta Sikora¹, Piotr Laidler³

Affiliations

¹ Department of Human Nutrition, Faculty of Food Technology, University of Agriculture in Krakow, Balicka 122, 30-149 Krakow, Poland.
² Department of Biochemistry and Molecular Biology, Medical Centre for Postgraduate Education, Marymoncka 99, 01-813 Warsaw, Poland.
³ Department of Medical Biochemistry, Jagiellonian University Medical College, Kopernika 7, 31-034 Krakow, Poland.

Abstract

In our previous study, we showed that fatty acids from CLA-enriched egg yolks (EFA-CLA) reduced the proliferation of breast cancer cells; however, the molecular mechanisms of their action remain unknown. In the current study, we used MCF-7 breast cancer cell line to determine the effect of EFA-CLA, as potential ligands for peroxisome proliferator-activated receptors (PPARs), on identified in silico PPAR-responsive genes: BCAR3, TCF20, WT1, ZNF621, and THRB (transcript TRβ2). Our results showed that EFA-CLA act as PPAR ligands with agonistic activity for all PPAR isoforms, with the highest specificity towards PPARγ. In conclusion, we propose that EFA-CLA-mediated regulation of PPAR-responsive genes is most likely facilitated by cis9,trans11CLA isomer incorporated in egg yolk. Notably, EFA-CLA activated PPAR more efficiently than nonenriched FA as well as synthetic CLA isomers. We also propose that this regulation, at least in part, can be responsible for the observed reduction in the proliferation of MCF-7 cells treated with EFA-CLA.