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Journal of Cancer Prevention

Original Article

Cancer prevention research 2009; 14(1): 20-27

Published online March 30, 2009

© Korean Society of Cancer Prevention

Effects of Tamoxifen and Ghrelin in ER-positive MCF-7 and ER-negative MDA-MB231 Breast Cancer Cells

Young Eun Choi1,2, Chang Hoon Cho1,2, Hye Ok Kim1,2, Yong Hwa Jo1,2, Jun-Kyu Song1,2, Hyung Hwan Baik1,2, Wonchae Choe1,2, Insug Kang1,2 and Kyung-Sik Yoon1,2

Abstract

Tamoxifen (Tam) is widely used in chemotherapy of breast cancer. It inhibits proliferation and induces apoptosis of breast cancer cells by estrogen receptor (ER)-dependent modulation of gene expression. ER involves with AMPK and MAPK pathway. Ghrelin is growth hormone and binds to growth hormone secreatagogue receptor1 (GHSR-1) that have estrogen receptor similar pathway. We studied to Tamoxifen, Estadiol & Ghrelin effects by MTT assay for cell viability and western blot for ERK/p38 phosphorylation in ER-positive MCF-7 (ER+) and ER-negative MDA-MB231 (ER−). We showed to MCF-7 cell death induction by Tamoxifen dose-dependent manner. But we can see inhibition of Tamoxifen effect by Estradiol and Ghrelin. ERK phosphorylation increased 2.9∼18.5-fold by dose-dependent Tamoxifen in both ER+ MCF-7 cells and 7.8-fold by 7ՌM Tamoxifen treatment in ER− MDA-MB231 cells. ERK phosphorylation was induced by Estadiol and Ghrelin in only ER+ MCF-7 cells, but p38 phosphorylation was not affected by Estradiol, Ghrelin and Tamoxifen in breast cancer cells. In conclusion, ERK activation of MAPK by Tamoxifen for cell death and Ghrelin in ER-positive MCF-7 cell line was observed. (Cancer Prev Res 14, 20-27, 2009)

Keywords: MCF7, MDA-MB231, Breast cancer, Tamoxifen, Ghrelin, Estrogen receptor

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