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

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 microM and 50 microM 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.

• Authors: Zhiwei Huang, Guichen Chen, Ping Shi
• Journal: Archives of pharmacal research (Arch Pharm Res) Vol. 31 Issue 6 Pg. 742-8 (Jun 2008) ISSN: 0253-6269 [Print] Korea (South)
• PMID: 18563356 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antineoplastic Agents, Phytogenic
• BAX protein, human
• Proto-Oncogene Proteins c-bcl-2
• bcl-2-Associated X Protein
• Cytochromes c
• Emodin

Topics

• Antineoplastic Agents, Phytogenic (pharmacology)
• Apoptosis (drug effects)
• Breast Neoplasms (metabolism, pathology)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Cell Shape (drug effects)
• Cytochromes c (metabolism)
• Dose-Response Relationship, Drug
• Emodin (pharmacology)
• Female
• Flow Cytometry
• Humans
• Mitochondria (drug effects, enzymology, metabolism, pathology)
• Proto-Oncogene Proteins c-bcl-2 (metabolism)
• Signal Transduction (drug effects)
• Time Factors
• bcl-2-Associated X Protein (metabolism)