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Inhibitory effect of sorafenib and arsenic trioxide on the FLT3ITD -mutated myelomonocytic leukemia MV-4-11 cells
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Abstract:
Objective : To determine the effect of the FLT3-specific inhibitor sorafenib in combination with arsenic trioxide on the proliferation, cell cycle and apoptosis of leukemia MV-4-11 cells，a biphenotypic B myelomonocytic leukemia cell line with FLT3-ITD mutations, as a model in vitro. Methods: Logarithmic phase MV-4-11 cells were cultured in the absence (control) or presence of sorafenib (1, 10, 100, 1 000, 5 000, 10 000 nmol/L), arsenic trioxide (0.125,0.25,0.5,1.0,2.0 μmol/L), and sorafenib (10 μmol/L) and arsenic trioxide (1.0 μmol/L) in combination, respectively, for 48 h cell proliferation was assessed by CCK-8 assay, apoptosis and cell cycle progression by flow cytometry. Results: Sorafenib and arsenic trioxide, each alone, inhibited MV-4-11 cell proliferation in a concentration dependent manner. However, the inhibitory effect was more significant (P<0.01) when 10 nmol/L sorafenib and 1.0 μmol/L arsenic trioxide were used in combination (\[70.72±1.03\]%) than each alone (\[47.24±1.27\]% and \[20.28±0.70\]%); the interaction coefficient for these two drugs was 0.696. Sorafenib alone resulted in cell cycle arrest in G0/G1 phase and sorafenib in combination with arsenic trioxide increased cell cycle arrest. Similarly, both sorafenib and arsenic trioxide induced MV-4-11 cell apoptosis, but they were more effective in combination than each in itself (89.06% vs 6827%, 7871%; P<0.05). Conclusion: Sorafenib and arsenic trioxide, each in itself, are capable of inhibiting proliferation, blocking cycle progression, and induing apoptosis in FLT3-mutated myeloid leukemia cells.
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Project Supported:
Project supported by the Science and Technology Progrom from Health Bureau of Jiangxi Province (No. 053035)
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