Abstract 4466: Celastrol induces apoptosis through modulation of estrogen receptor in human breast cancer cells

Abstract

Abstract Celastrol, a triterpene extracted from the Chinese medicine, is known to inhibit the growth of human prostate cancer cells. However, the anticancer activity of celastrol has not been reported in other cancer types. In this study, we investigated a negative role of celastrol in breast cancer development. We first examined the effects of celastrol on breast cancer cell growth. Results showed that celastrol inhibited estradiol-stimulated growth of MCF7 and T47D cells and increased apoptosis of breast cancer cells in a dose and time dependent manner. We also observed that celastrol decreased the expression of estrogen receptor (ER) at the both mRNA and protein levels in MCF7 and T47D human breast cancer cells. Results from the luciferase assay showed that the transcriptional activity of ER was decreased by the treatment with celastrol. Also, celastrol inhibited ER-mediated signaling and led to cell cycle arrest, which were confirmed by the expressions of cyclin D1 and progesterone receptor. We report that celastrol, an anticancer drug extracted from natural sources, induces apoptosis through modulation of estrogen receptor in human breast cancer cells and is a candidate for cancer chemotherapy in breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4466.