ZFP36L1 promotes monocyte/macrophage differentiation by repressing CDK6.
作者： Ming-Tai Chen , Lei Dong , Xin-Hua Zhang , Xiao-Lin Yin , Hong-Mei Ning
DOI: 10.1038/SREP16229
关键词:
摘要: RNA binding proteins (RBPs)-mediated post-transcriptional control has been implicated in influencing various aspects of metabolism and playing important roles mammalian development pathological diseases. However, the functions specific RBPs molecular mechanisms through which they act monocyte/macrophage differentiation remain to be determined. In this study, bioinformatics analysis experimental validation, we identify that ZFP36L1, a member ZFP36 zinc finger protein family, exhibits significant decrease acute myeloid leukemia (AML) patients compared with normal controls remarkable time-course increase during PMA-induced THP-1 HL-60 cells as well induction culture CD34(+) hematopoietic stem/progenitor (HSPCs). Lentivirus-mediated gain loss function assays demonstrate ZFP36L1 acts positive regulator participate differentiation. Mechanistic investigation further reveals binds CDK6 mRNA 3'untranslated region bearing adenine-uridine rich elements negatively regulates expression is subsequently demonstrated impede vitro HSPCs. Collectively, our work unravels ZFP36L1-mediated regulatory circuit repressing differentiation, may also provide therapeutic target for AML therapy.
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