期刊
MEDICINAL CHEMISTRY
卷 14, 期 1, 页码 60-66出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1573406413666170620091543
关键词
AKT; acute myeloid leukemia; apoptosis; cell cycle; ERK; nitidine chloride
资金
- National Nature Science Foundation of China [81300419, 91442126, 81370662, 81200377, 81400118]
- Taishan Scholars Program
- Fundamental Research Funds of Shandong University [2014JC026]
- Scientific and Technologic Development Programme of Shandong Medical and Health [2013WSB20019]
- Shandong Provincial Key Research and Development Plan [2015GSF118119]
- Science Foundation of Qilu Hospital of Shandong University [2015QLMS04, 2016QLQN30]
- Shandong University
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 time-dependent 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.
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