ABSTRACT
AIM: To investigate the expression of cystic fibrosis transmembrane conductance regulator (CFTR) in acute myeloid leukemia (AML) and its effect on the biological function of human erythroleukemia cell line TF1, and to explore the underlying mechanism .METHODS: The abundance of CFTR in the bone marrow mononuclear cells of patients with AML was measured by real-time PCR.After TF1 cells were incubated with CFTR specific inhibitor CFTRinh-172, cell viability, cell cycle distribution and cell apoptosis were analyzed by CCK-8 assay and flow cytometry . The Wnt signaling pathway-related proteins were determined by Western blot .RESULTS: CFTR was highly expressed in both patients with AML and leukemia cell lines .After incubated with CFTRinh172, the viability of TF1 cells was de-creased, the proportion of the cells in G0/G1 phase was increased, while that in S phase declined (P<0.05).Further-more, the cells treated with CFTRinh-172 exhibited higher apoptotic rate , accompanied with lower protein expression of β-catenin, c-Myc and cyclin D1 (P<0.05).CONCLUSION:CFTR expression is dramatically increased in AML .Inhibi-tion of CFTR restrains the growth and promotes the apoptosis of TF 1 cells via classical Wnt signaling pathway .