EBF1 Promotes Cell Proliferation, Migration and Inhibits Cell Apoptosis in AML

Background: Multiple studies reported that EBF1 played important roles in types of cancers. However, the potential molecular regulatory mechanism of EBF1 in acute myeloid leukemia (AML) remains to be further defined. In this study, we aimed to clarify the role and potential mechanism of EBF1 in AML.

Method: The expression levels of EBF1 were assessed in AML patients and cell lines by RT-qPCR and western blots. The expression of EBF1 was up-regulated or knocked down in AML cell lines by lentivirus mediated overexpression and RNA interference. CCK-8, flow cytometry and trans well assays were used to analyze the effect of EBF1 on cell proliferation, cycle, apoptosis and migration.

Results: The level of EBF1 expression was up-regulated in newly diagnosed AML patients and cell lines. The EBF1 gene expression significantly reduced in CR patients and significantly increased in relapsed patients as compared to newly diagnosed AML patients (both P <0.001). EBF1 knockdown repressed cell proliferation, migration, and induced cell apoptosis and cell cycle G0/G1 inhibition in AML cells. EBF1 overexpression promoted the malignancy of AML cells.

Conclusion: Our findings manifested that EBF1 was remarkably upregulated in AML and downregulation of EBF1 repressed the malignant behaviors of AML cells, which would provide a new insight for the treatment of AML.

No relevant conflicts of interest to declare.