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17 results on '"Brachet-Botineau, Marie"'

3. Dibenzofuran Derivatives Inspired from Cercosporamide as Dual Inhibitors of Pim and CLK1 Kinases

Author

Dao, Viet Hung, primary, Ourliac-Garnier, Isabelle, additional, Logé, Cédric, additional, McCarthy, Florence O., additional, Bach, Stéphane, additional, da Silva, Teresinha Gonçalves da, additional, Denevault-Sabourin, Caroline, additional, Thiéfaine, Jérôme, additional, Baratte, Blandine, additional, Robert, Thomas, additional, Gouilleux, Fabrice, additional, Brachet-Botineau, Marie, additional, Bazin, Marc-Antoine, additional, and Marchand, Pascal, additional

Published
2021
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4. Design, synthesis, and antiproliferative effect of 2,9‐bis[4‐(pyridinylalkylaminomethyl)phenyl]‐1,10‐phenanthroline derivatives on human leukemic cells by targeting G‐quadruplex

Author

Guillon, Jean, primary, Denevault‐Sabourin, Caroline, additional, Chevret, Edith, additional, Brachet‐Botineau, Marie, additional, Milano, Vittoria, additional, Guédin‐Beaurepaire, Aurore, additional, Moreau, Stéphane, additional, Ronga, Luisa, additional, Savrimoutou, Solène, additional, Rubio, Sandra, additional, Ferrer, Jacky, additional, Lamarche, Jeremy, additional, Mergny, Jean‐Louis, additional, Viaud‐Massuard, Marie‐Claude, additional, Ranz, Matthieu, additional, Largy, Eric, additional, Gabelica, Valérie, additional, Rosu, Frédéric, additional, Gouilleux, Fabrice, additional, and Desplat, Vanessa, additional

Published
2021
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5. Drug delivery system for platinum-based drugs

Author

Lollo, Giovanna, Benoit, Jean-Pierre, Brachet-Botineau, Marie, Micro et Nanomédecines Translationnelles (MINT), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Laboratoire d'automatique, de génie des procédés et de génie pharmaceutique (LAGEPP), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-École Supérieure Chimie Physique Électronique de Lyon-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), ERL 7001 LNOx (Leukemic Niche & redOx metabolism / Niche leucémique et métabolisme redOx) (LNOx), Groupe innovation et ciblage cellulaire (GICC), EA 7501 [2018-...] (GICC EA 7501), Université de Tours (UT)-Université de Tours (UT)-Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), Lemaire, Laurent, and Université de Tours-Université de Tours-Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire de Tours (CHRU TOURS)

Subjects
[SDV.SP.MED] Life Sciences [q-bio]/Pharmaceutical sciences/Medication, [SDV.SP.MED]Life Sciences [q-bio]/Pharmaceutical sciences/Medication
Abstract

The present invention concerns the nanomedicine field for anticancer therapy. The treatment of cancer using plat¬ inum-based compounds comprises certain drawbacks such as biocompatibility, loading efficacy, leakage of drugs during storage and in the bloodstream, more particularly due to the nature of the nanocarriers for platinum delivery. The inventors found that a novel nanosystem allows improving platinum-based drug in vivo performance, kinetics and efficacy. In particular, the present invention re¬ lates to nanoparticles useful as drug delivery system, said nanoparticles being formed from at least: (a) platinum-based drug, (b) poly-L-arginine, and (c) hyaluronic acid. Particularly, the inventors tested these nanoparticles in terms of entrapment efficiency and also carried out in vitro experiments in 2D cell culture (viability studies o B6KPC3, A549 and HT-29 cells) and 3D cell model (spheroids made of HTC-1 16) and in vivo experiments (by injecting intravenously to mice said nanoparticles or comparative oxaliplatin solution) to prove their efficiency.

Published
2020

6. Pharmacological Inhibition of Oncogenic STAT3 and STAT5 Signaling in Hematopoietic Cancers

Author

Brachet-Botineau, Marie, Polomski, Marion, Neubauer, Heidi, Juen, Ludovic, Hédou, Damien, Viaud-Massuard, Marie-Claude, Prié, Gildas, Gouilleux, Fabrice, Groupe innovation et ciblage cellulaire (GICC), EA 7501 [2018-...] (GICC EA 7501), Université de Tours, Chimie Organique et Bioorganique : Réactivité et Analyse (COBRA), Institut Normand de Chimie Moléculaire Médicinale et Macromoléculaire (INC3M), Institut de Chimie du CNRS (INC)-École Nationale Supérieure d'Ingénieurs de Caen (ENSICAEN), Normandie Université (NU)-Normandie Université (NU)-Institut national des sciences appliquées Rouen Normandie (INSA Rouen Normandie), Institut National des Sciences Appliquées (INSA)-Normandie Université (NU)-Institut National des Sciences Appliquées (INSA)-Université Le Havre Normandie (ULH), Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS)-Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Institut de Chimie du CNRS (INC)-École Nationale Supérieure d'Ingénieurs de Caen (ENSICAEN), Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie Organique Fine (IRCOF), Université de Rouen Normandie (UNIROUEN), Institut National des Sciences Appliquées (INSA)-Normandie Université (NU)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), and Université de Tours (UT)

Subjects
stat5, hematopoietic cancers, hemic and lymphatic diseases, [CHIM]Chemical Sciences, therapeutic targeting, [SDV.CAN]Life Sciences [q-bio]/Cancer, Review, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, lcsh:RC254-282, stat3, pharmacological inhibitors
Abstract

International audience; Signal Transducer and Activator of Transcription (STAT) 3 and 5 are important effectors of cellular transformation, and aberrant STAT3 and STAT5 signaling have been demonstrated in hematopoietic cancers. STAT3 and STAT5 are common targets for different tyrosine kinase oncogenes (TKOs). In addition, STAT3 and STAT5 proteins were shown to contain activating mutations in some rare but aggressive leukemias/lymphomas. Both proteins also contribute to drug resistance in hematopoietic malignancies and are now well recognized as major targets in cancer treatment. The development of inhibitors targeting STAT3 and STAT5 has been the subject of intense investigations during the last decade. This review summarizes the current knowledge of oncogenic STAT3 and STAT5 functions in hematopoietic cancers as well as advances in preclinical and clinical development of pharmacological inhibitors.

Published
2020

7. Acriflavine targets oncogenic STAT5 signaling in myeloid leukemia cells

Author

Hallal, Rawan, Nehme, Rawan, Brachet‐Botineau, Marie, Nehme, Ali, Dakik, Hassan, Deynoux, Margaux, Dello Sbarba, Persio, Levern, Yves, Zibara, Kazem, Gouilleux, Fabrice, Mazurier, Frédéric, ERL 7001 LNOx (Leukemic Niche & redOx metabolism / Niche leucémique et métabolisme redOx) (LNOx), Groupe innovation et ciblage cellulaire (GICC), EA 7501 [2018-...] (GICC EA 7501), Université de Tours-Université de Tours-Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire de Tours (CHRU TOURS), Laboratory of Stem Cells [Lebanese, Beirut] (ER045-PRASE), Lebanese University [Beirut] (LU), Università degli Studi di Firenze = University of Florence [Firenze] (UNIFI), Infectiologie et Santé Publique (UMR ISP), Université de Tours-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Lebanese University, Ligue Contre le Cancer, Lebanese National Council for Scientific Research, Hubert Curien Program, Region Centre-Val de Loire, Association 'CANCEN', Fondation de France, Université de Tours (UT)-Université de Tours (UT)-Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), and Université de Tours (UT)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)

Subjects
Carcinogenesis, chronic myeloid leukaemia, Down-Regulation, Antineoplastic Agents, [SDV.CAN]Life Sciences [q-bio]/Cancer, digestive system, acriflavine, resistance, Cell Line, Tumor, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, hemic and lymphatic diseases, STAT5 Transcription Factor, Humans, Protein Kinase Inhibitors, neoplasms, STAT5, Cell Proliferation, Tumor Suppressor Proteins, apoptosis, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, Original Articles, digestive system diseases, Drug Resistance, Neoplasm, [SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology, Original Article, cell cycle, K562 Cells, Signal Transduction
Abstract

International audience; Acriflavine (ACF) is an antiseptic with anticancer properties, blocking the growth of solid and haematopoietic tumour cells. Moreover, this compound has been also shown to overcome the resistance of cancer cells to chemotherapeutic agents. ACF has been shown to target hypoxia-inducible factors (HIFs) activity, which are key effectors of hypoxia-mediated chemoresistance. In this study, we showed that ACF inhibits the growth and survival of chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) cell lines in normoxic conditions. We further demonstrated that ACF down-regulates STAT5 expression in CML and AML cells but activates STAT3 in CML cells in a HIF-independent manner. In addition, we demonstrated that ACF suppresses the resistance of CML cells to tyrosine kinase inhibitors, such as imatinib. Our data suggest that the dual effect of ACF might be exploited to eradicate de novo or acquired resistance of myeloid leukaemia cells to chemotherapy.

Published
2020

8. New Quinoxaline Derivatives as Dual Pim-1/2 Kinase Inhibitors: Design, Synthesis and Biological Evaluation

Author

Oyallon, Bruno, primary, Brachet-Botineau, Marie, additional, Logé, Cédric, additional, Robert, Thomas, additional, Bach, Stéphane, additional, Ibrahim, Sajida, additional, Raoul, William, additional, Croix, Cécile, additional, Berthelot, Pascal, additional, Guillon, Jean, additional, Pinaud, Noël, additional, Gouilleux, Fabrice, additional, Viaud-Massuard, Marie-Claude, additional, and Denevault-Sabourin, Caroline, additional

Published
2021
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11. Oncogenic STAT5 signaling promotes oxidative stress in chronic myeloid leukemia cells by repressing antioxidant defenses

Author

Bourgeais, Jerome, Ishac, Nicole, Medrzycki, Magdalena, Brachet-Botineau, Marie, Desbourdes, Laura, Gouilleux-Gruart, Valérie, Pecnard, Emmanuel, Rouleux-Bonnin, Florence, Gyan, Emmanuel, Domenech, Jorge, Mazurier, Frédéric, Moriggl, Richard, Bunting, Kevin, Herault, Olivier, Gouilleux, Fabrice, Génétique, immunothérapie, chimie et cancer (GICC), UMR 7292 CNRS [2012-2017] (GICC UMR 7292 CNRS), Université de Tours (UT)-Centre National de la Recherche Scientifique (CNRS), Développement normal et pathologique des lymphocytes et signalisation, Université de Picardie Jules Verne (UPJV)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'hématologie, Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), Medizinische Universität Wien = Medical University of Vienna, Gouilleux, Fabrice, Université de Picardie Jules Verne (UPJV)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Université de Tours-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV.MHEP.HEM] Life Sciences [q-bio]/Human health and pathology/Hematology, Fusion Proteins, bcr-abl, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, Cell Cycle Checkpoints, Catalase, Models, Biological, Antioxidants, Oxidative Stress, [SDV.CAN] Life Sciences [q-bio]/Cancer, chronic myeloid leukemia, Cell Line, Tumor, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, hemic and lymphatic diseases, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], STAT5 Transcription Factor, Humans, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Reactive Oxygen Species, STAT5, Glutaredoxins, Research Paper, Bcr-Abl, Signal Transduction
Abstract

International audience; STAT5 transcription factors are frequently activated in hematopoietic neoplasms and are targets of various tyrosine kinase oncogenes. Evidences for a crosstalk between STAT5 and reactive oxygen species (ROS) metabolism have recently emerged but mechanisms involved in STAT5-mediated regulation of ROS still remain elusive. We demonstrate that sustained activation of STAT5 induced by Bcr-Abl in chronic myeloid leukemia (CML) cells promotes ROS production by repressing expression of two antioxidant enzymes, catalase and glutaredoxin-1(Glrx1). Downregulation of catalase and Glrx1 expression was also observed in primary cells from CML patients. Catalase was shown not only to reduce ROS levels but also, to induce quiescence in Bcr-Abl-positive leukemia cells. Furthermore, reduction of STAT5 phosphorylation and upregulation of catalase and Glrx1 were also evidenced in leukemia cells co-cultured with bone marrow stromal cells to mimic a leukemic niche. This caused downregulation of ROS levels and enhancement of leukemic cell quiescence. These data support a role of persistent STAT5 signaling in the regulation of ROS production in myeloid leukemias and highlight the repression of antioxidant defenses as an important regulatory mechanism.

Published
2017

12. Impact of cathepsin B-sensitive triggers and hydrophilic linkers onin vitroefficacy of novel site-specific antibody–drug conjugates

Author

Bryden, Francesca, primary, Martin, Camille, additional, Letast, Stéphanie, additional, Lles, Eva, additional, Viéitez-Villemin, Inmaculada, additional, Rousseau, Anaïs, additional, Colas, Cyril, additional, Brachet-Botineau, Marie, additional, Allard-Vannier, Emilie, additional, Larbouret, Christel, additional, Viaud-Massuard, Marie-Claude, additional, and Joubert, Nicolas, additional

Published
2018
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14. Oncogenic STAT5 signaling promotes oxidative stress in chronic myeloid leukemia cells by repressing antioxidant defenses

Author

Bourgeais, Jerome, primary, Ishac, Nicole, additional, Medrzycki, Magdalena, additional, Brachet-Botineau, Marie, additional, Desbourdes, Laura, additional, Gouilleux-Gruart, Valerie, additional, Pecnard, Emmanuel, additional, Rouleux-Bonnin, Florence, additional, Gyan, Emmanuel, additional, Domenech, Jorge, additional, Mazurier, Frederic, additional, Moriggl, Richard, additional, Bunting, Kevin D., additional, Herault, Olivier, additional, and Gouilleux, Fabrice, additional

Published
2016
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16. Acriflavine targets oncogenic STAT5 signaling in myeloid leukemia cells.

Author

Hallal R, Nehme R, Brachet-Botineau M, Nehme A, Dakik H, Deynoux M, Dello Sbarba P, Levern Y, Zibara K, Gouilleux F, and Mazurier F

Subjects
Antineoplastic Agents pharmacology, Carcinogenesis genetics, Cell Line, Tumor, Cell Proliferation drug effects, Cell Proliferation genetics, Down-Regulation drug effects, Down-Regulation genetics, Drug Resistance, Neoplasm drug effects, Drug Resistance, Neoplasm genetics, Humans, K562 Cells, Protein Kinase Inhibitors pharmacology, Acriflavine pharmacology, Carcinogenesis drug effects, Leukemia, Myelogenous, Chronic, BCR-ABL Positive drug therapy, Leukemia, Myelogenous, Chronic, BCR-ABL Positive genetics, STAT5 Transcription Factor genetics, Signal Transduction drug effects, Tumor Suppressor Proteins genetics
Abstract

Acriflavine (ACF) is an antiseptic with anticancer properties, blocking the growth of solid and haematopoietic tumour cells. Moreover, this compound has been also shown to overcome the resistance of cancer cells to chemotherapeutic agents. ACF has been shown to target hypoxia-inducible factors (HIFs) activity, which are key effectors of hypoxia-mediated chemoresistance. In this study, we showed that ACF inhibits the growth and survival of chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) cell lines in normoxic conditions. We further demonstrated that ACF down-regulates STAT5 expression in CML and AML cells but activates STAT3 in CML cells in a HIF-independent manner. In addition, we demonstrated that ACF suppresses the resistance of CML cells to tyrosine kinase inhibitors, such as imatinib. Our data suggest that the dual effect of ACF might be exploited to eradicate de novo or acquired resistance of myeloid leukaemia cells to chemotherapy., (© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

Published
2020
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17. Oncogenic STAT5 signaling promotes oxidative stress in chronic myeloid leukemia cells by repressing antioxidant defenses.

Author

Bourgeais J, Ishac N, Medrzycki M, Brachet-Botineau M, Desbourdes L, Gouilleux-Gruart V, Pecnard E, Rouleux-Bonnin F, Gyan E, Domenech J, Mazurier F, Moriggl R, Bunting KD, Herault O, and Gouilleux F

Subjects
Catalase metabolism, Cell Cycle Checkpoints genetics, Cell Line, Tumor, Fusion Proteins, bcr-abl genetics, Fusion Proteins, bcr-abl metabolism, Glutaredoxins genetics, Glutaredoxins metabolism, Humans, Leukemia, Myelogenous, Chronic, BCR-ABL Positive genetics, Leukemia, Myelogenous, Chronic, BCR-ABL Positive pathology, Models, Biological, Reactive Oxygen Species metabolism, Antioxidants metabolism, Leukemia, Myelogenous, Chronic, BCR-ABL Positive metabolism, Oxidative Stress, STAT5 Transcription Factor metabolism, Signal Transduction
Abstract

STAT5 transcription factors are frequently activated in hematopoietic neoplasms and are targets of various tyrosine kinase oncogenes. Evidences for a crosstalk between STAT5 and reactive oxygen species (ROS) metabolism have recently emerged but mechanisms involved in STAT5-mediated regulation of ROS still remain elusive. We demonstrate that sustained activation of STAT5 induced by Bcr-Abl in chronic myeloid leukemia (CML) cells promotes ROS production by repressing expression of two antioxidant enzymes, catalase and glutaredoxin-1(Glrx1). Downregulation of catalase and Glrx1 expression was also observed in primary cells from CML patients. Catalase was shown not only to reduce ROS levels but also, to induce quiescence in Bcr-Abl-positive leukemia cells. Furthermore, reduction of STAT5 phosphorylation and upregulation of catalase and Glrx1 were also evidenced in leukemia cells co-cultured with bone marrow stromal cells to mimic a leukemic niche. This caused downregulation of ROS levels and enhancement of leukemic cell quiescence. These data support a role of persistent STAT5 signaling in the regulation of ROS production in myeloid leukemias and highlight the repression of antioxidant defenses as an important regulatory mechanism.

Published
2017
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