5 results on '"David Hannebique"'
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2. Macrophage-Colony-Stimulating Factor Receptor Enhances Prostate Cancer Cell Growth and Aggressiveness In Vitro and In Vivo and Increases Osteopontin Expression
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Alexandra Mougel, Eric Adriaenssens, Boris Guyot, Lu Tian, Stéphanie Gobert, Thierry Chassat, Philippe Persoons, David Hannebique, Hélène Bauderlique-Le Roy, Jérôme Vicogne, Xuefen Le Bourhis, and Roland P. Bourette
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M-CSF ,CSF-1 receptor ,prostate ,C2H cell line ,TRAMP ,osteopontin ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
Prostate cancer is a major public health concern and one of the most prevalent forms of cancer worldwide. The definition of altered signaling pathways implicated in this complex disease is thus essential. In this context, abnormal expression of the receptor of Macrophage Colony-Stimulating Factor-1 (M-CSF or CSF-1) has been described in prostate cancer cells. Yet, outcomes of this expression remain unknown. Using mouse and human prostate cancer cell lines, this study has investigated the functionality of the wild-type CSF-1 receptor in prostate tumor cells and identified molecular mechanisms underlying its ligand-induced activation. Here, we showed that upon CSF-1 binding, the receptor autophosphorylates and activates multiple signaling pathways in prostate tumor cells. Biological experiments demonstrated that the CSF-1R/CSF-1 axis conferred significant advantages in cell growth and cell invasion in vitro. Mouse xenograft experiments showed that CSF-1R expression promoted the aggressiveness of prostate tumor cells. In particular, we demonstrated that the ligand-activated CSF-1R increased the expression of spp1 transcript encoding for osteopontin, a key player in cancer development and metastasis. Therefore, this study highlights that the CSF-1 receptor is fully functional in a prostate cancer cell and may be a potential therapeutic target for the treatment of prostate cancer.
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- 2022
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3. Use of 2,6-diaminopurine as a potent suppressor of UGA premature stop codons in cystic fibrosis
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Catherine Leroy, Sacha Spelier, Nadège Charlene Essonghe, Virginie Poix, Rebekah Kong, Patrick Gizzi, Claire Bourban, Séverine Amand, Christine Bailly, Romain Guilbert, David Hannebique, Philippe Persoons, Gwenaëlle Arhant, Anne Prévotat, Philippe Reix, Dominique Hubert, Michèle Gérardin, Mathias Chamaillard, Natalia Prevarskaya, Sylvie Rebuffat, George Shapovalov, Jeffrey Beekman, Fabrice Lejeune, Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 (CANTHER), Institut Pasteur de Lille, and Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS)
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Pharmacology ,[SDV]Life Sciences [q-bio] ,Drug Discovery ,Genetics ,Molecular Medicine ,Molecular Biology - Abstract
International audience; Nonsense mutations are responsible for around 10% of cases of genetic diseases, including cystic fibrosis. 2,6-diaminopurine (DAP) has recently been shown to promote efficient readthrough of UGA premature stop codons. In this study, we show that DAP can correct a nonsense mutation in the Cftr gene in vivo in a new CF mouse model, in utero, and through breastfeeding, thanks, notably, to adequate pharmacokinetic properties. DAP turns out to be very stable in plasma and is distributed throughout the body. The ability of DAP to correct various endogenous UGA nonsense mutations in the CFTR gene and to restore its function in mice, in organoids derived from murine or patient cells, and in cells from patients with cystic fibrosis reveals the potential of such readthrough-stimulating molecules in developing a therapeutic approach. The fact that correction by DAP of certain nonsense mutations reaches a clinically relevant level, as judged from previous studies, makes the use of this compound all the more attractive.
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- 2023
4. 2,6-Diaminopurine as a highly potent corrector of UGA nonsense mutations
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Catherine Leroy, Séverine Amand, Anthony Mouray, David Tulasne, Andreas E. Kulozik, Christine Bailly, Thierry Chassat, Carole Trzaska, David Hannebique, Eric Adriaenssens, Jean-Michel Saliou, Elisabeth Werkmeister, Pierre-Arthur Moreau, Eric Westhof, Evelyne Duvernois-Berthet, Yuri Motorin, Romain Guilbert, Marie-Christine Copin, Virginie Marchand, Sylvie Rebuffat, Fabrice Lejeune, Hana Benhabiles, Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 (CANTHER), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Molécules de Communication et Adaptation des Micro-organismes (MCAM), Muséum national d'Histoire naturelle (MNHN)-Centre National de la Recherche Scientifique (CNRS), Ingénierie, Biologie et Santé en Lorraine (IBSLor), Université de Lorraine (UL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Physiologie moléculaire et adaptation (PhyMA), Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 (CIIL), Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Université de Lille-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Réseau International des Instituts Pasteur (RIIP), Laboratoire de Génie civil et Géo-environnement (LGCgE), Ecole nationale supérieure Mines-Télécom Lille Douai (IMT Lille Douai), Institut Mines-Télécom [Paris] (IMT)-Institut Mines-Télécom [Paris] (IMT)-Université de Lille-Université d'Artois (UA)-Université catholique de Lille (UCL)-École polytechnique universitaire de Lille (Polytech Lille), Hopp Children's Cancer Center Heidelberg [Heidelber, Germany] (KITZ), German Cancer Research Center - Deutsches Krebsforschungszentrum [Heidelberg] (DKFZ)-Heidelberg University Hospital [Heidelberg], Architecture et Réactivité de l'ARN (ARN), Institut de biologie moléculaire et cellulaire (IBMC), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Ingénierie Moléculaire et Physiopathologie Articulaire (IMoPA), Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), F.L. is an Inserm researcher supported by fundings from Vaincre la mucoviscidose, the Association française contre les myopathies, the GIP Cancéropôle Nord Ouest, the Fondation Maladies Rares and the SATT Lutech, Authors would like to thank Dr. Jens Lykke-Andersen, Pr. P.A. Jänne and Pr. Lynne Maquat for reagents, Dr. Clément Carré, Dr. Bruno Lapeyre, Dr. Gabriele Neu-Yilik, Dr. Matthias Hentze, and Dr. Jean-Paul Renaud for helpful discussions. Authors also thank the Bicel facility for technical help, the PLEHTA for technical help on mouse managing and in vivo experiments, Valérie IGEL-BOURGUIGNON and Dr. Lilia AYADI from the Next-Generation Sequencing Core Facility of UMS2008 IBSLor (Université de Lorraine-CNRS-INSERM) for their help in RiboMethSeq library preparation and sequencing., Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers [Lille] (CANTHER), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Université Lille Nord (France)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), Centre d’Infection et d’Immunité de Lille (CIIL) - U1019 - UMR 8204 (CIIL), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Department of Pediatric Oncology, Alder Hey Children's Hospital, Alder Hey Children's Hospital, Centre National de la Recherche Scientifique (CNRS)-Institut de biologie moléculaire et cellulaire (IBMC), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Médecine cellulaire et molécualire, PRES Université Lille Nord de France-Institut de Biologie de Lille-IFR 142, Université d'Artois (UA)-École polytechnique universitaire de Lille (Polytech Lille)-Université de Lille-Ecole nationale supérieure Mines-Télécom Lille Douai (IMT Lille Douai), Institut Mines-Télécom [Paris] (IMT)-Institut Mines-Télécom [Paris] (IMT)-Yncréa Hauts-de-France, and Université catholique de Lille (UCL)-Université catholique de Lille (UCL)
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0301 basic medicine ,Molecular biology ,General Physics and Astronomy ,chemistry.chemical_compound ,Mice ,RNA, Transfer ,lcsh:Science ,2-Aminopurine ,ComputingMilieux_MISCELLANEOUS ,Genetics ,Regulation of gene expression ,tRNA Methyltransferases ,Multidisciplinary ,Molecular medicine ,Drug discovery ,Lepisma ,3. Good health ,Gene Expression Regulation, Neoplastic ,Drug screening ,Codon, Nonsense ,Cytosine ,Science ,Nonsense mutation ,Mice, Nude ,Biology ,General Biochemistry, Genetics and Molecular Biology ,Article ,03 medical and health sciences ,[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN] ,Animals ,Humans ,Gene ,RNA metabolism ,030102 biochemistry & molecular biology ,2,6-Diaminopurine ,HEK 293 cells ,fungi ,RNA ,[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology ,General Chemistry ,Genes, p53 ,Disease Models, Animal ,030104 developmental biology ,HEK293 Cells ,chemistry ,Cancer cell ,Mutation ,lcsh:Q ,Drug Screening Assays, Antitumor ,HeLa Cells - Abstract
Nonsense mutations cause about 10% of genetic disease cases, and no treatments are available. Nonsense mutations can be corrected by molecules with nonsense mutation readthrough activity. An extract of the mushroom Lepista inversa has recently shown high-efficiency correction of UGA and UAA nonsense mutations. One active constituent of this extract is 2,6-diaminopurine (DAP). In Calu-6 cancer cells, in which TP53 gene has a UGA nonsense mutation, DAP treatment increases p53 level. It also decreases the growth of tumors arising from Calu-6 cells injected into immunodeficient nude mice. DAP acts by interfering with the activity of a tRNA-specific 2′-O-methyltransferase (FTSJ1) responsible for cytosine 34 modification in tRNATrp. Low-toxicity and high-efficiency UGA nonsense mutation correction make DAP a good candidate for the development of treatments for genetic diseases caused by nonsense mutations., Nonsense mutations can be corrected by several molecules that activate readthrough of premature termination codon. Here, the authors report that 2,6-diaminopurine efficiently corrects UGA nonsense mutations with no significant toxicity.
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- 2020
5. The out-of-field dose in radiation therapy induces delayed tumorigenesis by senescence evasion
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Erwan Goy, Maxime Tomezak, Caterina Facchin, Nathalie Martin, Emmanuel Bouchaert, Jerome Benoit, Clementine de Schutter, Joe Nassour, Laure Saas, Claire Drullion, Priscille M Brodin, Alexandre Vandeputte, Olivier Molendi-Coste, Laurent Pineau, Gautier Goormachtigh, Olivier Pluquet, Albin Pourtier, Fabrizio Cleri, Eric Lartigau, Nicolas Penel, Corinne Abbadie, Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 (CANTHER), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Institut d’Électronique, de Microélectronique et de Nanotechnologie - UMR 8520 (IEMN), Centrale Lille-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-JUNIA (JUNIA), Université catholique de Lille (UCL)-Université catholique de Lille (UCL), Oncovet Clinical Research [Loos] (Eurasanté - OCR), Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 (CIIL), Réseau International des Instituts Pasteur (RIIP), Physique - IEMN (PHYSIQUE - IEMN), Université catholique de Lille (UCL)-Université catholique de Lille (UCL)-Centrale Lille-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-JUNIA (JUNIA), Centre Régional de Lutte contre le Cancer Oscar Lambret [Lille] (UNICANCER/Lille), Université de Lille-UNICANCER, This work was supported by the Centre National de la Recherche Scientifique, the Université de Lille, the Ligue contre le Cancer (Comité du Pas-de-Calais, Comité de la Somme, Comité du Nord), the Cancéropole Nord-Ouest, the Institut Pasteur de Lille, the SIRIC OncoLille (Grant INCa-DGOS-Inserm 6041), the Agence Nationale de Recherche (ANR-10-EQPX-04-01), the Feder (12001407 [D-AL]), and the Contrat de Plan Etat Région CPER Cancer 2015-2020. EG had a fellowship from the Institut Pasteur de Lille and the Région Hauts-de-France. MT had a fellowship from the Université de Lille. CF had a fellowship from the European Erasmus program. JN had fellowships from the Université de Lille and from the Association pour la Recherche sur le Cancer. LS and CD had fellowships from the Région Hauts-de-France. We thank Thomas Lacornerie for giving access to the Varian CLINAC and for performing dose profiles. We thank the Bioimaging Center Lille-Nord de France (Campus Calmette), especially Antonino Bongiovanni and Hélène Bauderlique, for imaging and cytometry facilities. We thank the PLETHA animal facility, especially Thierry Chassat and David Hannebique. We thank David Dombrowicz for giving access to the BD Influx (Becton Dickinson). We thank Benoit Vatrinet, Anaïs Engrand, and Olivier Samyn for technical help. The authors have no conflicting financial interests., FundingLigue Contre le CancerCorinne AbbadieSIRIC Oncolille (INCa-DGOS-Inserm 6041)Corinne AbbadieAgence Nationale de la Recherche (ANR-10-EQPX-04-01)Priscille M BrodinFeder (12001407 (D-AL))Priscille M BrodinInstitut Pasteur de Lille, France (PhD student Fellowship)Erwan GoyRegion des Hauts-de-France, France (PhD student Fellowship)Erwan GoyEuropean Erasmus Program (Graduate student Fellowship)Caterina FacchinFondation ARC pour la Recherche sur le Cancer (PhD student Fellowship)Joe NassourRegion des Hauts-de-France (Engineer Fellowship)Laure SaasRegion des Hauts-de-France (Post-doctoral Fellowship)Claire Drullion, and CLERI, FABRIZIO
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DNA Repair ,General Immunology and Microbiology ,Carcinogenesis ,General Neuroscience ,Neoplasms, Second Primary ,[SDV.CAN]Life Sciences [q-bio]/Cancer ,General Medicine ,[SDV.IB.MN]Life Sciences [q-bio]/Bioengineering/Nuclear medicine ,General Biochemistry, Genetics and Molecular Biology ,[SDV.IB.MN] Life Sciences [q-bio]/Bioengineering/Nuclear medicine ,Mice ,Cell Transformation, Neoplastic ,[SDV.CAN] Life Sciences [q-bio]/Cancer ,Animals ,DNA Breaks, Single-Stranded ,Cellular Senescence ,DNA Damage - Abstract
International audience; A rare but severe complication of curative-intent radiation therapy is the induction of second primary cancers. These cancers preferentially develop not inside the planning target volume (PTV) but around, over several centimeters, after a latency period of 1–40 years. We show here that normal human or mouse dermal fibroblasts submitted to the out-of-field dose scattering at the margin of a PTV receiving a mimicked patient’s treatment do not die but enter in a long-lived senescent state resulting from the accumulation of unrepaired DNA single-strand breaks, in the almost absence of double-strand breaks. Importantly, a few of these senescent cells systematically and spontaneously escape from the cell cycle arrest after a while to generate daughter cells harboring mutations and invasive capacities. These findings highlight single-strand break-induced senescence as the mechanism of second primary cancer initiation, with clinically relevant spatiotemporal specificities. Senescence being pharmacologically targetable, they open the avenue for second primary cancer prevention.
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- 2022
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