ArticleLeukemia2010
Elevated PIN1 expression by C/EBPalpha-p30 blocks C/EBPalpha-induced granulocytic differentiation through c-Jun in AML.
Article in Leukemia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 54 citations in OpenAlex.
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- PIN1P1 is activated by CREB1 and promotes gastric cancer progression via interacting with YBX1 and upregulating PIN1.Journal of cellular and molecular medicine · 2024Article
- Development of a contacting transwell co-culture system for theFrontiers in cell and developmental biology · 2023Article
- Targeting peptidyl-prolyl isomerase 1 in experimental pulmonary arterial hypertension.The European respiratory journal · 2022Article
- Targeting Pin1 for Modulation of Cell Motility and Cancer Therapy.Biomedicines · 2021Review
- Gain-of-Function Effects of N-Terminal CEBPA Mutations in Acute Myeloid Leukemia.BioEssays : news and reviews in molecular, cellular and developmental biology · 2020Review
- Targeting PIN-1 Attenuates GCB DLBCL Cell Proliferation Through Inhibition of PI3K/AKT Signaling.OncoTargets and therapy · 2020Article
- Prolyl Isomerase Pin1 in Human Cancer: Function, Mechanism, and Significance.Frontiers in cell and developmental biology · 2020Review
- Pinning Down the Transcription: A Role for Peptidyl-ProlylFrontiers in cell and developmental biology · 2020Review
- Prolyl isomerization of FAAP20 catalyzed by PIN1 regulates the Fanconi anemia pathway.PLoS genetics · 2019Article
- Inhibition of Casein Kinase 2 Disrupts Differentiation of Myeloid Cells in Cancer and Enhances the Efficacy of Immunotherapy in Mice.Cancer research · 2018Article
- Prolyl isomerase Pin1: a promoter of cancer and a target for therapy.Cell death & disease · 2018Review
- BCR-ABL enhances the prolyl isomerase activity of Pin 1 by interacting with DAPK1 in phCancer medicine · 2018Article
- Pin1 inhibition exerts potent activity against acute myeloid leukemia through blocking multiple cancer-driving pathways.Journal of hematology & oncology · 2018Article
- [Roles of CCAAT enhancer binding protein α in acute myeloblastic leukemia].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018Review
- Gears-In-Motion: The Interplay of WW and PPIase Domains in Pin1.Frontiers in oncology · 2018Review
- C/EBPα deregulation as a paradigm for leukemogenesis.Leukemia · 2017Review
- c-Myc suppresses miR-451⊣YWTAZ/AKT axis via recruiting HDAC3 in acute myeloid leukemia.Oncotarget · 2016Article
- The presence of C/EBPα and its degradation are both required for TRIB2-mediated leukaemia.Oncogene · 2016Article
- The isomerase PIN1 controls numerous cancer-driving pathways and is a unique drug target.Nature reviews. Cancer · 2016Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
Abstract
The transcription factor CCAAT enhancer-binding protein alpha (C/EBPalpha) has an important role in granulopoiesis. The tumor suppressor function of C/EBPalpha is shown by the findings that loss of expression or function of C/EBPalpha in leukemic blasts contributes to a block in myeloid cell differentiation and to leukemia. C/EBPalpha mutations are found in around 9% of acute myeloid leukemia (AML) patients. The mechanism by which the mutant form of C/EBPalpha (C/EBPalpha-p30) exerts a differentiation block is not well understood. By using a proteomic screen, we have recently reported PIN1 as a target of C/EBPalpha-p30 in AML. In the present study, we show that C/EBPalpha-p30 induces PIN1 expression. We observed elevated PIN1 expression in leukemic patient samples. Induction of C/EBPalpha-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/EBPalpha 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/EBPalpha. Our data suggest that the inhibition of PIN1 could be a potential strategy of treating AML patients with C/EBPalpha mutation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.