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• W2042076653 abstract "The transcription factor CCAAT enhancer-binding protein α (C/EBPα) has an important role in granulopoiesis. The tumor suppressor function of C/EBPα is shown by the findings that loss of expression or function of C/EBPα in leukemic blasts contributes to a block in myeloid cell differentiation and to leukemia. C/EBPα mutations are found in around 9% of acute myeloid leukemia (AML) patients. The mechanism by which the mutant form of C/EBPα (C/EBPα-p30) exerts a differentiation block is not well understood. By using a proteomic screen, we have recently reported PIN1 as a target of C/EBPα-p30 in AML. In the present study, we show that C/EBPα-p30 induces PIN1 expression. We observed elevated PIN1 expression in leukemic patient samples. Induction of C/EBPα-p30 results in recruitment of E2F1 in the PIN1 promoter. We show that the inhibition of PIN1 leads to myeloid differentiation in primary AML blasts with C/EBPα mutations. Overexpression of PIN1 in myeloid cells leads to block of granulocyte differentiation. We also show that PIN1 increases the stability of the c-Jun protein by inhibiting c-Jun ubiquitination, and c-Jun blocks granulocyte differentiation mediated by C/EBPα. Our data suggest that the inhibition of PIN1 could be a potential strategy of treating AML patients with C/EBPα mutation." @default.
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• W2042076653 date "2010-04-08" @default.
• W2042076653 modified "2023-10-13" @default.
• W2042076653 title "Elevated PIN1 expression by C/EBPα-p30 blocks C/EBPα-induced granulocytic differentiation through c-Jun in AML" @default.
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• W2042076653 doi "https://doi.org/10.1038/leu.2010.37" @default.
• W2042076653 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2923485" @default.
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