Archives of Pharmacal Research

, Volume 31, Issue 6, pp 742–748

Emodin-induced apoptosis in human breast cancer BCap-37 cells through the mitochondrial signaling pathway

Authors

  • Zhiwei Huang
    • Northwest Institute of Plateau BiologyChinese Academy of Sciences
  • Guichen Chen
    • Northwest Institute of Plateau BiologyChinese Academy of Sciences
    • Northwest Institute of Plateau BiologyChinese Academy of Sciences
Articles Drug Efficacy and Safety

DOI: 10.1007/s12272-001-1221-6

Cite this article as:
Huang, Z., Chen, G. & Shi, P. Arch. Pharm. Res. (2008) 31: 742. doi:10.1007/s12272-001-1221-6

Abstract

Emodin, a natural anthraquinone compound isolated from the rhizome of rhubarb, is reported to suppress the growth of tumor in many clinical situations. In this study, we focused on the effect of emodin in human breast cancer BCap-37 cells and further understand the underlying molecular mechanism in treating breast cancer. Using MTT assay and flow cytometry, we demonstrated the critical role of emodin in the suppression of the proliferation of BCap-37 cells based on a concentration-and time-dependent manner. The increase of apoptotic rate was also observed after incubation of BCap-37 cells on emodin at 20 μM and 50 μM for 48 h. The cells exhibited typical apoptotic features including cellular morphological change, chromatin condensation and membrane blebbing. The results of the study further showed that Bcl-2 level decreased, while Bax and cytosolic cytochrome c levels in sample cells increased after the emodin treatment by using Western blot. The decline in the Bcl-2/Bax ratio and the increase of cytosolic cytochrome c concentration were consistent with the increase of the apoptotic ratio. The results strongly suggest that the disruption of the mitochondrial signaling pathway was involved in emodin-induced apoptosis in BCap-37 cells.

Key words

EmodinHuman breast cancer BCap-37 cellsApoptosisThe mitochondrial signaling pathway
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Copyright information

© The Pharmaceutical Society of Korea 2008