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Biotechnol Lett. 2009 Apr;31(4):487-94. doi: 10.1007/s10529-008-9888-x. Epub 2008 Nov 28.

Microarray and biochemical analysis of bufalin-induced apoptosis of HL-60 Cells.

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Medical Systems Biology Research Center, Tsinghua University School of Medicine, Beijing 100084, People's Republic of China.


Bufalin is a natural toxin with anti-leukemic properties. It induces cell differentiation and apoptosis, as well as increasing the sensitivity of leukemia cells to other chemotherapeutic agents. We investigated the biological effects and molecular mechanisms of bufalin triggered apoptosis in HL-60 cells by gene expression profiling. The broad transcriptional response to bufalin was consistent with bufalin's action of regulating HL-60 cell proliferation and apoptosis, as well as its synergistic effect with other drugs. Further transcription factor ELISA experiments suggested that the transcription factors NFkappaB and AP-1 were activated to promote bufalin-induced HL-60 cell apoptosis. Our study provides new insights into the molecular mechanisms of bufalin, might prove to be beneficial in leukemia therapy.

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