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

doi:10.1016/j.bbrc.2008.09.111

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

Department of Pharmaceutical Sciences

Research output: Contribution to journal › Article › peer-review

25 Scopus citations

Abstract

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 (ER_α) negatively interferes with PPARγ signaling in breast cancer cells. Here we show that ER_α inhihits PPARγ transactivity and ER_α-mediated inhibition of PPARγ transactivity is blocked by tamoxifen, an estrogen receptor blocker. The activation of ER_α with 17-β-estradiol blocked PPRE transactivity induced by troglitazone, a PPARγ ligand, indicating the resistance of ER_α-positive breast cancer cells to troglitazone. Indeed, troglitazone inhibited the growth of ER_α-negative MDA-MB-231 cells more than that of ER_α-positive MCF-7 cells. Combination of troglitazone with tamoxifen led to a marked increase in growth inhibition of ER_α-positive MCF-7 cells compared to either agent alone. Our data indicates that troglitazone enhances the growth inhibitory activity of tamoxifen in ER_α-positive MCF-7 cells.

Original language	English
Pages (from-to)	242-247
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	377
Issue number	1
DOIs	https://doi.org/10.1016/j.bbrc.2008.09.111
State	Published - 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.

Keywords

Apoptosis
Breast cancer
ER
PPARγ ligand
Tamoxifen

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbrc.2008.09.111

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@article{64ae92dfaaa24caba079d7f92148c9df,

title = "Troglitazone enhances tamoxifen-induced growth inhibitory activity of MCF-7 cells",

abstract = "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.",

keywords = "Apoptosis, Breast cancer, ER, PPARγ ligand, Tamoxifen",

author = "Yu, {Hong Nu} and Noh, {Eun Mi} and Lee, {Young Rae} and Roh, {Si Gyun} and Song, {Eun Kyung} and Han, {Myung Kwan} and Lee, {Yong Chul} and Shim, {In Kyong} and Lee, {Seung Jin} and Jung, {Sung Hoo} and Kim, {Jong Suk} and Youn, {Hyun Jo}",

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.",

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AU - Yu, Hong Nu

AU - Noh, Eun Mi

AU - Lee, Young Rae

AU - Roh, Si Gyun

AU - Song, Eun Kyung

AU - Han, Myung Kwan

AU - Lee, Yong Chul

AU - Shim, In Kyong

AU - Lee, Seung Jin

AU - Jung, Sung Hoo

AU - Kim, Jong Suk

AU - Youn, Hyun Jo

N1 - 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.

PY - 2008/12/5

Y1 - 2008/12/5

N2 - 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.

AB - 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.

KW - Apoptosis

KW - Breast cancer

KW - ER

KW - PPARγ ligand

KW - Tamoxifen

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ER -

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

Abstract

Bibliographical note

Keywords

UN SDGs

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