Troglitazone enhances tamoxifen-induced growth inhibitory activity of MCF-7 cells

Hong-Nu Yu, Eun-Mi Noh, Young-Rae Lee, Si-Gyun Roh, Eun-Kyung Song, Myung-Kwan Han, Yong-Chul Lee, In Kyong Shim, Seung Jin Lee, Sung Hoo Jung, Jong-Suk Kim, Hyun Jo Youn
Biochemical and Biophysical Research Communications 2008 December 5, 377 (1): 242-7
Peroxisome proliferator-activated receptor gamma (PPARgamma) ligands have been identified as a potential source of therapy for human cancers. However, PPARgamma ligands have a limitation for breast cancer therapy, since estrogen receptor alpha (ER(alpha)) negatively interferes with PPARgamma signaling in breast cancer cells. Here we show that ER(alpha) inhihits PPARgamma transactivity and ER(alpha)-mediated inhibition of PPARgamma transactivity is blocked by tamoxifen, an estrogen receptor blocker. The activation of ER(alpha) with 17-beta-estradiol blocked PPRE transactivity induced by troglitazone, a PPARgamma ligand, indicating the resistance of ER(alpha)-positive breast cancer cells to troglitazone. Indeed, troglitazone inhibited the growth of ER(alpha)-negative MDA-MB-231 cells more than that of ER(alpha)-positive MCF-7 cells. Combination of troglitazone with tamoxifen led to a marked increase in growth inhibition of ER(alpha)-positive MCF-7 cells compared to either agent alone. Our data indicates that troglitazone enhances the growth inhibitory activity of tamoxifen in ER(alpha)-positive MCF-7 cells.

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