دورية أكاديمية
أعرض في EDS

Translation efficiency driven by CNOT3 subunit of the CCR4-NOT complex promotes leukemogenesis.

التفاصيل البيبلوغرافية
العنوان: Translation efficiency driven by CNOT3 subunit of the CCR4-NOT complex promotes leukemogenesis.
المؤلفون: Ghashghaei M; Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada.; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada., Liu Y; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada.; Department of Experimental Medicine, University of British Columbia, Vancouver, Canada., Ettles J; CRUK Beatson Institute, Glasgow, UK.; School of Cancer Sciences, University of Glasgow, Glasgow, UK., Bombaci G; Department of Medicine, Indiana University Simon Comprehensive Cancer Center, Indianapolis, IN, USA., Ramkumar N; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada., Liu Z; Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada.; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada., Escano L; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada., Miko SS; Genome Sciences Centre, British Columbia Cancer Research Centre, Vancouver, Canada., Kim Y; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada.; Bioinformatics program, University of British Columbia, Vancouver, Canada., Waldron JA; CRUK Beatson Institute, Glasgow, UK.; School of Cancer Sciences, University of Glasgow, Glasgow, UK., Do K; Memorial Sloan Kettering Cancer Center, New York, NY, USA., MacPherson K; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada., Yuen KA; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada., Taibi T; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada., Yue M; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada., Arsalan A; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada., Jin Z; Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada.; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada., Edin G; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada., Karsan A; Genome Sciences Centre, British Columbia Cancer Research Centre, Vancouver, Canada., Morin GB; Genome Sciences Centre, British Columbia Cancer Research Centre, Vancouver, Canada.; Department of Medical Genetics, University of British Columbia, Vancouver, Canada., Kuchenbauer F; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada., Perna F; Department of Medicine, Indiana University Simon Comprehensive Cancer Center, Indianapolis, IN, USA.; Department of Blood and Marrow Transplant and Cellular Immunotherapy, Moffit Cancer Center, Tampa, FL, USA., Bushell M; CRUK Beatson Institute, Glasgow, UK.; School of Cancer Sciences, University of Glasgow, Glasgow, UK., Vu LP; Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada. ly.vu@ubc.ca.; Terry Fox Laboratory, British Columbia Cancer Research Centre Vancouver, Vancouver, Canada. ly.vu@ubc.ca.
المصدر: Nature communications [Nat Commun] 2024 Mar 15; Vol. 15 (1), pp. 2340. Date of Electronic Publication: 2024 Mar 15.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : Nature Pub. Group
مواضيع طبية MeSH: Leukemia, Myeloid, Acute*/genetics , Proteomics* , Transcription Factors*/genetics , Transcription Factors*/metabolism, Humans ; Carcinogenesis/genetics ; Cell Differentiation ; Receptors, CCR4
مستخلص: Protein synthesis is frequently deregulated during tumorigenesis. However, the precise contexts of selective translational control and the regulators of such mechanisms in cancer is poorly understood. Here, we uncovered CNOT3, a subunit of the CCR4-NOT complex, as an essential modulator of translation in myeloid leukemia. Elevated CNOT3 expression correlates with unfavorable outcomes in patients with acute myeloid leukemia (AML). CNOT3 depletion induces differentiation and apoptosis and delayed leukemogenesis. Transcriptomic and proteomic profiling uncovers c-MYC as a critical downstream target which is translationally regulated by CNOT3. Global analysis of mRNA features demonstrates that CNOT3 selectively influences expression of target genes in a codon usage dependent manner. Furthermore, CNOT3 associates with the protein network largely consisting of ribosomal proteins and translation elongation factors in leukemia cells. Overall, our work elicits the direct requirement for translation efficiency in tumorigenesis and propose targeting the post-transcriptional circuitry via CNOT3 as a therapeutic vulnerability in AML.
(© 2024. The Author(s).)
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معلومات مُعتمدة: P30 CA008748 United States CA NCI NIH HHS; Scholar Award American Society of Hematology (ASH); Special Fellow Leukemia and Lymphoma Society (Leukemia & Lymphoma Society)
المشرفين على المادة: 0 (CCR4 protein, human)
0 (CNOT3 protein, human)
0 (Receptors, CCR4)
0 (Transcription Factors)
تواريخ الأحداث: Date Created: 20240316 Date Completed: 20240318 Latest Revision: 20240516
رمز التحديث: 20240516
مُعرف محوري في PubMed: PMC10943099
DOI: 10.1038/s41467-024-46665-2
PMID: 38491013
قاعدة البيانات: MEDLINE
الوصف
تدمد:2041-1723
DOI:10.1038/s41467-024-46665-2