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

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


Peroxisome proliferator-activated receptor γ (PPARγ) ligands have been identified as a potential source of therapy for human cancers. However, PPARγ ligands have a limitation for breast cancer therapy, since estrogen receptor α (ERα) negatively interferes with PPARγ signaling in breast cancer cells. Here we show that ERα inhihits PPARγ transactivity and ERα-mediated inhibition of PPARγ transactivity is blocked by tamoxifen, an estrogen receptor blocker. The activation of ERα with 17-β-estradiol blocked PPRE transactivity induced by troglitazone, a PPARγ ligand, indicating the resistance of ERα-positive breast cancer cells to troglitazone. Indeed, troglitazone inhibited the growth of ERα-negative MDA-MB-231 cells more than that of ERα-positive MCF-7 cells. Combination of troglitazone with tamoxifen led to a marked increase in growth inhibition of ERα-positive MCF-7 cells compared to either agent alone. Our data indicates that troglitazone enhances the growth inhibitory activity of tamoxifen in ERα-positive MCF-7 cells.

Original languageEnglish
Pages (from-to)242-247
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number1
StatePublished - 5 Dec 2008

Bibliographical note

Funding Information:
This work was supported in part by research funds from the Chonbuk National University Hospital Research Institute of Clinical Medicine, Korea Breast Cancer Foundation, the Korea Science and Engineering Foundation (M10528010003-05N2801-00310), and a grant of the Post-Doc. Program, Chonbuk National University.


  • Apoptosis
  • Breast cancer
  • ER
  • PPARγ ligand
  • Tamoxifen


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