Novel tumor-suppressor FOXN3 is downregulated in adult acute myeloid leukemia.

Forkhead box protein N3 (FOXN3) is a transcriptional repressor involved in cell cycle regulation and tumorigenesis. Abnormalities in gene structure and epigenetics of FOXN3 are closely associated with the occurrence of hematological malignancies; however, its involvement in the pathogenesis of acute myeloid leukemia (AML) remains unknown. The present study aimed to examine the potential significance of FOXN3 in AML. FOXN3 expression levels were examined in patients with AML and AML cell lines, and its clinical significance in AML was evaluated. FOXN3-overexpressing AML cell lines were established, and the biological function of FOXN3 was detected by flow cytometry and a Cell Counting Kit-8 assay. A significant decrease in FOXN3 expression levels was observed in patients with AML and in the AML cell lines in vitro. FOXN3 expression levels were associated with the number of leukocytes in patients. FOXN3 overexpression may inhibit cell proliferation in AML cell lines, induce cell cycle S-phase arrest and promote apoptosis in OCI-AML3 and THP-AML cells. The present study provided insight into how FOXN3 may serve as a novel tumor suppressor in AML.