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Oncol Rep. 2014 Dec;32(6):2527-32. doi: 10.3892/or.2014.3535. Epub 2014 Oct 10.

Celastrol induces the apoptosis of breast cancer cells and inhibits their invasion via downregulation of MMP-9.

Author information

1
Molecular Cancer Research Center, Yanbian University, Yanji, Jilin 133002, P.R. China.
2
Key Laboratory of Natural Resources of Changbai Mountain and Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji, Jilin 133002, P.R. China.
3
Department of Pharmacy, Jilin Province People's Hospital, Changchun, Jilin 130021, P.R. China.

Abstract

Celastrol is a quinone methide triterpene derived from Tripterygium wilfordii Hook F., a plant used in traditional medicine. In the present study, we reported that celastrol potentiated tumor necrosis factor-α (TNF-α)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2). In addition, celastrol significantly reduced the invasion of MDA-MB-231 human breast cancer cells after TNF-α stimulation. As matrix metalloproteinase-9 (MMP-9) plays a critical role in tumor metastasis, we analyzed its expression with celastrol treatment. Western blot analysis and real-time PCR showed that celastrol dose-dependently suppressed TNF-α-induced MMP-9 gene expression at both the mRNA and protein levels in MDA-MB-231 cells. Taken together, our findings indicate that celastrol may be a potential candidate for breast cancer chemotherapy.

PMID:
25310109
DOI:
10.3892/or.2014.3535
[Indexed for MEDLINE]

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