Background: Acute myeloid leukemia (AML) is the most common hematological malignancy
in adults, characterized by distorted proliferation and development of myeloid cells and
their precursors in the bone marrow. Nitidine chloride, a naturally occurring alkaloid, has been
identified to possess antitumor activity. However, the effects of nitidine chloride on acute myeloid
leukemia cells and its underlying mechanisms have not been elucidated. Here we investigated the
cellular and molecular mechanism of the anti-leukemic effects of nitidine chloride.
Methods and Results: Nitidine chloride treatment for 48 consecutive hours exhibited a timedependent
and dose-dependent growth inhibition activity against AML cells by inducing cell cycle
arrest and apoptosis. Moreover, nitidine chloride downregulated Cyclin B1, CDK1 and Bcl-2,
upregulated p27 and Bax, inactivated PARP, activated Caspase-3 in AML cells. We further demonstrated
that growth inhibition activity of nitidine chloride in AML cells is partially via inhibiting
the phosphorylation of AKT and ERK.
Conclusion: In conclusion, our data suggest that nitidine chloride could be an effective therapeutic
agent against AML via cell cycle arrest and apoptosis.