Determination of differentially regulated proteins upon proteasome inhibition in AML cell lines by the combination of large-scale and targeted quantitative proteomics

التفاصيل البيبلوغرافية
العنوان: Determination of differentially regulated proteins upon proteasome inhibition in AML cell lines by the combination of large-scale and targeted quantitative proteomics
المؤلفون: Mariette Matondo, Bernard Monsarrat, Odile Burlet-Schiltz, Marlène Marcellin, Marie-Pierre Bousquet-Dubouch, Karima Chaoui, Anne Gonzalez-de-Peredo
المساهمون: Institut de pharmacologie et de biologie structurale (IPBS), Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, The work was supported in part by grants from the Région Midi‐Pyrénées, the 'Fondation pour la Recherche Médicale' (programme Grands Equipements), European Fonds (FEDER), Toulouse metropole, 'Fond Social Européen' (FSE) and the 'Ligue contre le cancer' Grants., We thank Dr. Darragh O'Brien from Institut Pasteur for the careful reading of this manuscript., We thank members of the group for insightful comments related to this work. We would like to thank David Bouyssié for MFPAQ software and technical support. We would like also to thank our collaborators Stephane Manenti, for discussion. We Thanks Pr. Dr. Ruedi Aebersold from IMSB (ETH Zurich) for allowing the SRM measurement on the TSQ Vantage., Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)
المصدر: Proteomics
Proteomics, Wiley-VCH Verlag, 2017, Applications and Developments in Targeted Proteomics, 17 (7), pp.1600089. ⟨10.1002/pmic.201600089⟩
بيانات النشر: HAL CCSD, 2017.
سنة النشر: 2017
مصطلحات موضوعية: 0301 basic medicine, MESH: Gene Ontology, Technology, Leupeptins, Cellular differentiation, Cell Cycle Proteins, Apoptosis, MESH: Cell Cycle / drug effects, Biochemistry, SILAC, MESH: Interleukins / metabolism, Bortezomib, MESH: Leukocytes / drug effects, Leukocytes, MESH: Interleukins / genetics, MESH: Apoptosis Regulatory Proteins / metabolism, Protein Isoforms, Proteasome inhibitor, Phosphorylation, MESH: Proteasome Endopeptidase Complex / drug effects, Targeted proteomics, Heat-Shock Proteins, MESH: Proteasome Endopeptidase Complex / metabolism, MESH: Computational Biology, Chemistry, Gene Expression Regulation, Leukemic, Cell Cycle, MESH: Apoptosis / drug effects, Cell Differentiation, Cell cycle, MESH: Phosphorylation / drug effects, MESH: Cell Cycle Proteins / metabolism, 3. Good health, Cell biology, MESH: Cell Cycle Proteins / genetics, MESH: Heat-Shock Proteins / genetics, Proteasome Inhibitors, medicine.drug, Research Article, Signal Transduction, MESH: Cell Differentiation, Proteasome Endopeptidase Complex, MESH: Cell Line, Tumor, Quantitative proteomics, MESH: Tumor Suppressor Protein p53 / metabolism, MESH: Protein Isoforms / genetics, MESH: Acetylcysteine / pharmacology, MESH: Molecular Sequence Annotation, MESH: Apoptosis Regulatory Proteins / genetics, MESH: Transcription Factors / genetics, MESH: Protein Isoforms / metabolism, 03 medical and health sciences, MESH: Gene Expression Profiling, MESH: Leukocytes / pathology, Heat shock protein, Cell Line, Tumor, medicine, MESH: Acetylcysteine / analogs & derivatives, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Cell Cycle Protein, Molecular Biology, MESH: Proteasome Inhibitors / pharmacology, MESH: Transcription Factors / metabolism, MESH: Humans, MESH: Leupeptins / pharmacology, Gene Expression Profiling, Interleukins, Computational Biology, Molecular Sequence Annotation, MESH: Bortezomib / pharmacology, MESH: Tumor Suppressor Protein p53 / genetics, MESH: Heat-Shock Proteins / metabolism, MESH: Leukocytes / metabolism, Acetylcysteine, 030104 developmental biology, Gene Ontology, Proteasome, MESH: Gene Expression Regulation, Leukemic / drug effects, Tumor Suppressor Protein p53, Apoptosis Regulatory Proteins, Human acute myeloid leukemia (AML) cells, Transcription Factors
الوصف: International audience; The ubiquitin-proteasome pathway (UPP) plays a critical role in the degradation of proteins implicated in cell cycle control, signal transduction, DNA damage response, apoptosis and immune response. Proteasome inhibitors can inhibit the growth of a broad spectrum of human cancer cells by altering the balance of intracellular proteins. However, the targets of these compounds in acute myeloid leukemia (AML) cells have not been fully characterized. Herein, we combined large-scale quantitative analysis by SILAC-MS and targeted quantitative proteomic analysis in order to identify proteins regulated upon proteasome inhibition in two AML cell lines displaying different stages of maturation: immature KG1a cells and mature U937 cells. In-depth data analysis enabled accurate quantification of more than 7000 proteins in these two cell lines. Several candidates were validated by selected reaction monitoring (SRM) measurements in a large number of samples. Despite the broad range of proteins known to be affected by proteasome inhibition, such as heat shock (HSP) and cell cycle proteins, our analysis identified new differentially regulated proteins, including IL-32, MORF family mortality factors and apoptosis inducing factor SIVA, a target of p53. It could explain why proteasome inhibitors induce stronger apoptotic responses in immature AML cells.
اللغة: English
تدمد: 1615-9853
1615-9861
DOI: 10.1002/pmic.201600089⟩
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b46ca49bbfe534e269c497edfc5fdec0
https://hal-pasteur.archives-ouvertes.fr/pasteur-02619400/document
Rights: OPEN
رقم الانضمام: edsair.doi.dedup.....b46ca49bbfe534e269c497edfc5fdec0
قاعدة البيانات: OpenAIRE
الوصف
تدمد:16159853
16159861
DOI:10.1002/pmic.201600089⟩