Abstract
The t(8;21)(q22;q22) translocation generated the fusion protein AML1-ETO. AML1-ETO recruits histone deacetylase (HDAC) complex via its ETO part to repress AML1-mediated transactivation. Our previous study demonstrated that HDAC inhibitor phenylbutyrate (PB) could induce AML1-ETO positive leukemia cell line Kasumi-1 cells to undergo differentiation and apoptosis accompanied by significant changes in gene expression profile. ZFP36L2 was one of the up-regulated genes in Kasumi-1 cells induced by PB treatment. In this study, ZFP36L2 was found to express at a lower level in acute myeloid leukemia (AML) patients with t(8;21) compared to AML patients without t(8;21). In order to investigate the correlation between the expression of ZFP36L2 and AML1 or AML1-ETO, the putative AML1 binding sites in the enhancer/promoter region of ZFP36L2 gene were predicted through the bioinformatics analysis. And the biological function of ZFP36L2 in leukemic cells was further investigated. The results demonstrated that AML1 could transactivate ZFP36L2 significantly by binding on specific site of the ZFP36L2 promoter sequence. And overexpression of ZFP36L2 in leukemia cells could inhibit the cell proliferation, promote cell-cycle arrest in G0/G1 phase and induce the cell apoptosis. In conclusion, ZFP36L2 could be transactivated by AML1, which subsequently induced cell-cycle arrest and apoptosis of leukemia cells.
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