Fig. 2.

Working model for the hypothesis that omega-3 fatty acids can inhibit progestin stimulation of breast cancer invasion. The model is separated into two parts for clarity. a Depicts progestin stimulation of invasion, while b diagrams omega-3 fatty acid pathways which may act to inhibit progestin stimulation of invasive properties. Necessarily, the model is incomplete, yet testable. Parts of the model are colored red to emphasize pathways for which there is the most evidence suggesting interaction of omega-3 fatty acid pathways to inhibit progestin-driven pathways, in particular progestin stimulation of MUC1. Small upward-pointing arrows to the right of gene products indicate up-regulation of these products, whereas downward-pointing arrows indicate down-regulation. Abbreviations: HSP heat shock proteins, PR progesterone receptor, P phosphate group, Src the tyrosine–protein kinase c-Src, Ras the G-protein Ras, EGFR epidermal growth factor receptor 1, EGF epidermal growth factor, MUC-1 mucin-1, TF tissue factor, MAPKs mitogen-activated protein kinases, MnSOD manganese superoxide dismutase, CXCR4 a transmembrane G-protein-coupled chemokine receptor for CXCL-12/stromal cell-derived factor 1, PPARγ peroxisome proliferator-activated receptor gamma, RXR retinoid X receptor, PPRE peroxisome proliferator response element, EZH2 enhancer of zeste homolog 2 (a histone-methylating polycomb group protein), ErbB-2/Her2 human epidermal growth factor receptor 2