Mechanism for the Differentiation of EoL-1 Cells into Eosinophils by Histone Deacetylase InhibitorsKaneko M.a · Ishihara K.a · Takahashi A.a · Hong J.a-c · Hirasawa N.a · Zee O.b · Ohuchi K.a, d
aLaboratory of Pathophysiological Biochemistry, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan; bLaboratory of Pharmacognosy, Graduate School of Pharmacy, Sungkyunkwan University, Suwon, Korea and cLaboratory of Pathophysiology, College of Pharmacy, Sookmyung Women’s University, Seoul, Korea; dFaculty of Pharmacy, Yasuda Woman’s University, Hiroshima, Japan
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Background: EoL-1 cells have a FIP1L1-PDGFRA fusion gene which causes the transformation of eosinophilic precursor cells into leukemia cells. Recently, we suggested that the induction of differentiation of EoL-1 cells into eosinophils by the HDAC inhibitors apicidin and n-butyrate is due to the continuous inhibition of HDACs. However, neither apicidin nor n-butyrate inhibited the expression of FIP1L1-PDGFRA mRNA, although both these inhibitors suppressed cell proliferation. Therefore, in this study, we analyzed whether the levels of FIP1L1-PDGFRα protein and phosphorylated-Stat5 involved in the signaling for the proliferation of EoL-1 cells are attenuated by HDAC inhibitors. Methods: EoL-1 cells were incubated in the presence of apicidin, TSA or n-butyrate. FIP1L1-PDGFRα and phosphorylated-Stat5 were detected by Western blotting. Results: Treatment of EoL-1 cells with apicidin at 100 nM or n-butyrate at 500 µM decreased the levels of FIP1L1-PDGFRα protein and phosphorylated-Stat5, while that with trichostatin A at 30 nM did not. Conclusions: The decrease in the level of FIP1L1-PDGFRα protein caused by apicidin and n-butyrate might be one of the mechanisms by which EoL-1 cells are induced to differentiate into eosinophils by these HDAC inhibitors.
© 2007 S. Karger AG, Basel
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