Reference - Detail
|Author||Kaneko M, Ishihara K, Takahashi A, Hong J, Hirasawa N, Zee O, Ohuchi K.|
|Title||Mechanism for the differentiation of EoL-1 cells into eosinophils by histone deacetylase inhibitors.|
|Journal||Int. Arch. Allergy Immunol.|
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-PDGFRalpha 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-PDGFRalpha and phosphorylated-Stat5 were detected by Western blotting.
RESULTS:Treatment of EoL-1 cells with apicidin at 100 nM or n-butyrate at 500 microM decreased the levels of FIP1L1-PDGFRalpha protein and phosphorylated-Stat5, while that with trichostatin A at 30 nM did not.
CONCLUSIONS:The decrease in the level of FIP1L1-PDGFRalpha 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.
|Volume||143 Suppl 1|
|MeSH||Butyrates / pharmacology* Cell Differentiation / drug effects Cell Differentiation / physiology Cell Line, Tumor / cytology Cell Line, Tumor / drug effects Eosinophils / cytology* Gene Expression Regulation, Leukemic / drug effects Histone Deacetylase Inhibitors* Humans Hydroxamic Acids / pharmacology Hypereosinophilic Syndrome / genetics Hypereosinophilic Syndrome / pathology* Neoplasm Proteins / biosynthesis Neoplasm Proteins / genetics Neoplasm Proteins / physiology* Oncogene Proteins, Fusion / biosynthesis Oncogene Proteins, Fusion / genetics Oncogene Proteins, Fusion / physiology* Peptides, Cyclic / pharmacology* Phosphorylation / drug effects Protein Processing, Post-Translational / drug effects RNA, Messenger / biosynthesis RNA, Messenger / genetics Receptor, Platelet-Derived Growth Factor alpha / biosynthesis Receptor, Platelet-Derived Growth Factor alpha / genetics Receptor, Platelet-Derived Growth Factor alpha / physiology* STAT5 Transcription Factor / metabolism mRNA Cleavage and Polyadenylation Factors / biosynthesis mRNA Cleavage and Polyadenylation Factors / genetics mRNA Cleavage and Polyadenylation Factors / physiology*|
|WOS Category||ALLERGY IMMUNOLOGY|
|Human and Animal Cells|