BACKGROUND: The mechanism of emodin-mediated cell apoptosis has been investigated extensively in many types of human cancer cells. Our previous study demonstrated that emodin induced apoptosis through the decrease of Bcl-2/Bax ratio and the increase of cytoplasm cytochrome c concentration in human breast cancer BCap-37 cells. However, emodin's reaction to breast cancer cells remains elusive. MATERIALS AND METHODS: An apoptosis-associated cDNA microarray comprised of 458 known genes, namely, death receptors, calpains, death kinases, granzymes, DNA fragmentation proteins, caspases and Bcl-2 family, was used to determine the impact of emodin in breast cancer BCap-37 cells. Furthermore, the candidate emodin target genes were further evaluated via real-time quantitative PCR and Western blot analysis. RESULTS: We found that gene expression profiling in human breast cancer BCap-37 cells was altered when exposed to emodin. Thirty of the unique genes that were either induced or repressed in response to emodin-induced apoptosis were also identified. A follow-up study characterized p53, emodin-induced gene, IGF-2, and emodin-repressed gene, and the downstream proteins were also seen as possible molecular targets of emodin. CONCLUSION: Data from this study provide novel evidence that emodin induces gene expression profiling changes, but has no effects on caspases. In addition, the p53 pathway may cooperate with the IGF-2 pathway, resulting in an emodin-induced apoptosis through disruption of the mitochondrial signaling pathway in BCap-37 cells.
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