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Icaritin induces AML cell apoptosis via the MAPK/ERK and PI3K/AKT signal pathways

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Abstract

Icaritin, a hydrolytic product of icaritin, is isolated from the traditional Chinese medicinal herb epimedium. Icaritin inhibits the proliferation of several tumor cell lines, but its effect on acute myeloid leukemia (AML) and underlying mechanisms remain to be identified. In the present study, we demonstrated that icaritin inhibits the proliferation of human AML cell lines NB4, HL60, and U937, in a dose- and time-dependent manner. Importantly, icaritin showed anti-leukemia activity on bone marrow mononuclear cells from 15 newly diagnosed AML patients. Flow cytometry analyses indicated that icaritin induces AML cells apoptosis. Icaritin induced activation of caspase-9, -3, -7 and the cleavage of PARP as measured by Western blotting. Icaritin downregulates p-ERK and p-AKT and inhibits the expression of c-myc. These results suggest that icaritin is a promising candidate drug for the treatment of AML. The underlying mechanisms of icaritin anti-AML activity are associated with inhibition of the MAPK/ERK and PI3K/AKT signals and downregulation of c-myc.

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Acknowledgments

This work was supported by the National Science and Technology Major Projects (2011ZX09302-007-04, 2012ZX09101215002), the Special Scientific Fund for Public Welfare Health Industry (201202017) and National Natural Science Foundation of China (81270635, 81070389).

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Correspondence to Jianxiang Wang.

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Li, Q., Huai, L., Zhang, C. et al. Icaritin induces AML cell apoptosis via the MAPK/ERK and PI3K/AKT signal pathways. Int J Hematol 97, 617–623 (2013). https://doi.org/10.1007/s12185-013-1317-9

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  • DOI: https://doi.org/10.1007/s12185-013-1317-9

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