The peroxisome proliferator-activated receptor (PPAR)-α-selective ligand hydroxyeicosatetraenoic acid (HETE) induces apoptosis in human breast cancer cell lines, which is potentiated by AGN194204

<p><b>Copyright information:</b></p><p>Taken from "A retinoid X receptor (RXR)-selective retinoid reveals that RXR-α is potentially a therapeutic target in breast cancer cell lines, and that it potentiates antiproliferative and apoptotic responses to peroxisome proliferator-activated receptor ligands"</p><p>Breast Cancer Research 2004;6(5):R546-R555.</p><p>Published online 23 Jul 2004</p><p>PMCID:PMC549174.</p><p>Copyright © 2004 Crowe et al.; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.</p> The indicated breast cancer cell lines were treated with vehicle (con), 100 μmol/l HETE, 100 nmol/l AGN194204 (AGN), or both compounds simultaneously (HETE+AGN) for 24 hours. The percentage of apoptotic cells was determined by dUTP nick-end labeling (TUNEL) assay and fluorescence microscopy. These experiments were performed three times, with similar results. Error bars indicate the standard error of the mean. The PPAR-α-selective ligand HETE activates the intrinsic apoptotic pathway in human breast cancer cell lines. Whole cell lysates from the indicated breast cancer cell lines treated with 100 μmol/l HETE for up to 24 hours were subjected to western blot, with anti-caspase (casp) and anti-β-actin antibodies shown on the left. Relative expression of each protein was determined using the same membrane. These experiments were performed three times, with similar results. Representative blots are shown