دورية أكاديمية
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The stress sensor GCN2 differentially controls ribosome biogenesis in colon cancer according to the nutritional context.

التفاصيل البيبلوغرافية
العنوان: The stress sensor GCN2 differentially controls ribosome biogenesis in colon cancer according to the nutritional context.
المؤلفون: Piecyk M; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Triki M; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Laval PA; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Duret C; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Fauvre J; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Cussonneau L; INRAE, Unité de Nutrition Humaine, UMR1019, Université Clermont Auvergne, Clermont-Ferrand, France., Machon C; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France.; Biochemistry and Pharmaco-Toxicology Laboratory, Lyon Sud Hospital, Hospices Civils de Lyon Pierre-Bénite, University Hospital of Lyon, France., Guitton J; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France.; Biochemistry and Pharmaco-Toxicology Laboratory, Lyon Sud Hospital, Hospices Civils de Lyon Pierre-Bénite, University Hospital of Lyon, France., Rama N; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Gibert B; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Ichim G; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Catez F; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Bourdelais F; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Durand S; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Diaz JJ; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Coste I; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Renno T; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Manié SN; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Aznar N; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Ansieau S; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France., Ferraro-Peyret C; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France.; Hospices Civils de Lyon, Plateforme AURAGEN, France., Chaveroux C; Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, France.
المصدر: Molecular oncology [Mol Oncol] 2023 Jul 15. Date of Electronic Publication: 2023 Jul 15.
Publication Model: Ahead of Print
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: John Wiley & Sons, Inc Country of Publication: United States NLM ID: 101308230 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1878-0261 (Electronic) Linking ISSN: 15747891 NLM ISO Abbreviation: Mol Oncol Subsets: MEDLINE
أسماء مطبوعة: Publication: 2017- : Hoboken, New Jersey : John Wiley & Sons, Inc.
Original Publication: Amsterdam : Elsevier
مستخلص: Nutrient availability is a key determinant of tumor cell behavior. While nutrient-rich conditions favor proliferation and tumor growth, scarcity, and particularly glutamine starvation, promotes cell dedifferentiation and chemoresistance. Here, linking ribosome biogenesis plasticity with tumor cell fate, we uncover that the amino acid sensor general control non-derepressible 2 (GCN2; also known as eIF-2-alpha kinase 4) represses the expression of the precursor of ribosomal RNA (rRNA), 47S, under metabolic stress. We show that blockade of GCN2 triggers cell death by an irremediable nucleolar stress and subsequent TP53-mediated apoptosis in patient-derived models of colon adenocarcinoma (COAD). In nutrient-rich conditions, a cell-autonomous GCN2 activity supports cell proliferation by stimulating 47S rRNA transcription, independently of the canonical integrated stress response (ISR) axis. Impairment of GCN2 activity prevents nuclear translocation of methionyl-tRNA synthetase (MetRS), resulting in nucleolar stress, mTORC1 inhibition and, ultimately, autophagy induction. Inhibition of the GCN2-MetRS axis drastically improves the cytotoxicity of RNA polymerase I (RNA pol I) inhibitors, including the first-line chemotherapy oxaliplatin, on patient-derived COAD tumoroids. Our data thus reveal that GCN2 differentially controls ribosome biogenesis according to the nutritional context. Furthermore, pharmacological co-inhibition of the two GCN2 branches and RNA pol I activity may represent a valuable strategy for elimination of proliferative and metabolically stressed COAD cells.
(© 2023 The Authors. Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.)
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معلومات مُعتمدة: CV-2021-039 Cancéropôle CLARA; CVPPRCAB000180 Cancéropôle CLARA; CVPPRCAN000174 Cancéropôle CLARA; NA-7-07-20 CNRS Prematuration; ARCMD-Doc22021020003295 Fondation ARC pour la Recherche sur le Cancer; R16173CC Fondation ARC pour la Recherche sur le Cancer; 17IA66ANR-PLASCAN-MEHLEN Institut Convergence François Rabelais; R17167CC Ligue Nationale contre le Cancer; R19007CC Ligue Nationale contre le Cancer; n_839398 The Marie Sklodowska-Curie Fellowship; 19-010898-01 Region Auvergne Rhone-Alpes; PLBIO22-227 Institut National Du Cancer; MERCK KGaA
فهرسة مساهمة: Keywords: GCN2; colon cancer; methionyl-tRNA synthetase; nucleolar stress; ribosome biogenesis
تواريخ الأحداث: Date Created: 20230715 Latest Revision: 20230819
رمز التحديث: 20230819
DOI: 10.1002/1878-0261.13491
PMID: 37452637
قاعدة البيانات: MEDLINE
الوصف
تدمد:1878-0261
DOI:10.1002/1878-0261.13491