Peroxisome proliferator‐activated receptor gamma as a molecular target of polyunsaturated fatty acids in breast cancer cells
TL;DRAbstract
Studies have shown that individual sources of dietary fat influence breast cancer development and growth. Linoleic acid (LAA) induces proliferation and other physiological responses in estrogen‐dependent breast cancer (MCF‐7) cells. However, how LAA elicits these effects remains unclear. We hypothesize that peroxisome proliferator‐activated receptor gamma (PPARγ ), which is over expressed in MCF‐7 cells, serves as a molecular target of LAA. The purpose of these studies was to examine whether LAA functions directly through PPARγ and to determine if LAA is itself a ligand of PPARγ. Utilizing a PPARγ response element (PPRE)‐mediated reporter construct, we demonstrate that LAA activates the reporter in MCF‐7 cells and that this effect is inhibited by GW 9662, a known PPARγ antagonist. We then expressed the receptor in a prostate cancer cell line (22Rv1) that is PPARγ negative. When these cells were co‐transfected with a PPARγ expression plasmid, LAA induced the PPRE‐reporter. Also, LAA ind
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Studies have shown that individual sources of dietary fat influence breast cancer development and growth. Linoleic acid (LAA) induces proliferation and other physiological responses in estrogen‐dependent breast cancer (MCF‐7) cells. However, how LAA elicits these effects remains unclear. We hypothesize that peroxisome proliferator‐activated receptor gamma (PPARγ ), which is over expressed in MCF‐7 cells, serves as a molecular target of LAA. The purpose of these studies was to examine whether LAA functions directly through PPARγ and to determine if LAA is itself a ligand of PPARγ. Utilizing a PPARγ response element (PPRE)‐mediated reporter construct, we demonstrate that LAA activates the reporter in MCF‐7 cells and that this effect is inhibited by GW 9662, a known PPARγ antagonist. We then expressed the receptor in a prostate cancer cell line (22Rv1) that is PPARγ negative. When these cells were co‐transfected with a PPARγ expression plasmid, LAA induced the PPRE‐reporter. Also, LAA ind
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