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

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Abstract

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 NFκB 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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Acknowledgements

This work was supported by the grant of the National Hi-Tech Program of China (No. 2006AA020701). We are grateful to Dr. De’an Guo of Peking University for providing the bufalin compound. We thank Hao Xu, Junxia Wei, Xiaohong Chen, Yahui Wang and Yonghong Ren for their excellent technical assistance. We thank Lihua Huang and Yong Guo for their helpful discussions. We also thank Dr. Xiaoxiang Zhu for critically reading the manuscript.

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Correspondence to Jing Cheng.

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Chen, A., Yu, J., Zhang, L. et al. Microarray and biochemical analysis of bufalin-induced apoptosis of HL-60 Cells. Biotechnol Lett 31, 487–494 (2009). https://doi.org/10.1007/s10529-008-9888-x

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  • DOI: https://doi.org/10.1007/s10529-008-9888-x

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