Send to

Choose Destination
Cancer Lett. 2011 Jan 1;300(1):57-65. doi: 10.1016/j.canlet.2010.09.006. Epub 2010 Oct 12.

Celastrol inhibits the growth of estrogen positive human breast cancer cells through modulation of estrogen receptor α.

Author information

School of Life Sciences and Biotechnology, Korea University, Seoul 136-701, South Korea.


Human estrogen receptor α (ERα) is a nuclear transcription factor that displays a major therapeutic target for breast cancer. The transcriptional activity of ERα can be regulated by particular estrogen receptor modulators. Celastrol, a quinine methide triterpene extracted from a Chinese medicine (Trypterygium wilfordii Hook F.), has been reported to have therapeutic efficacy against various cancer cells, including prostate cancer, leukemia, and melanoma cells. However, ERα regulation by Celastrol has not been reported. In this study, we investigated the effects of Celastrol on the growth of breast cancer cells. We observed that Celastrol decreased expression of ERα at both the mRNA and the protein levels in MCF7 and T47D human breast cancer cells. Results from a luciferase assay showed that Celastrol decreased the transcriptional activity of ERα. Also, Celastrol treatment inhibited ERα target gene expression, including expressions of cyclin D(1), progesterone receptor (PR), and c-Myb leading to cell cycle arrest and growth inhibition of breast cancer cells. We propose that Celastrol, an anti-cancer drug extracted from natural sources, induces inhibition of cell growth through modulation of ERα in estrogen positive breast cancer cells and is a candidate for use in cancer chemotherapy for human breast cancer.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center