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3. Chimeric protein EWS::FLI1 drives cell proliferation in Ewing Sarcoma via aberrant expression of KCNN1/SK1 and dysregulation of calcium signaling

Author

Dupuy, Maryne, Gueguinou, Maxime, Postec, Anaïs, Brion, Régis, Tesfaye, Robel, Mullard, Mathilde, Regnier, Laura, Amiaud, Jérôme, Hubsch, Clémence, Potier-Cartereau, Marie, Chantôme, Aurélie, Brounais-Le Royer, Bénédicte, Baud’huin, Marc, Georges, Steven, Lamoureux, François, Ory, Benjamin, Entz-Werlé, Natacha, Delattre, Olivier, Rédini, Françoise, Vandier, Christophe, and Verrecchia, Franck

Published
2024
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8. Ewing sarcoma from molecular biology to the clinic

Author

Dupuy, Maryne, primary, Lamoureux, François, additional, Mullard, Mathilde, additional, Postec, Anaïs, additional, Regnier, Laura, additional, Baud’huin, Marc, additional, Georges, Steven, additional, Brounais-Le Royer, Bénédicte, additional, Ory, Benjamin, additional, Rédini, Françoise, additional, and Verrecchia, Franck, additional

Published
2023
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9. Tracking Targets of Dynamic Super-Enhancers in Vitro to Better Characterize Osteoclastogenesis and to Evaluate the Effect of Diuron on the Maturation of Human Bone Cells

Author

Tesfaye, Robel A., primary, Lavaud, Melanie, additional, Charrier, Céline, additional, Brounais-Le Royer, Bénédicte, additional, Cartron, Pierre-François, additional, Verrecchia, Franck, additional, Baud’huin, Marc, additional, Lamoureux, François, additional, Georges, Steven, additional, and Ory, Benjamin, additional

Published
2023
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11. Supplementary Figure S2 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis

Author

Rodriguez Calleja, Lidia, primary, Jacques, Camille, primary, Lamoureux, François, primary, Baud'huin, Marc, primary, Tellez Gabriel, Marta, primary, Quillard, Thibaut, primary, Sahay, Debashish, primary, Perrot, Pierre, primary, Amiaud, Jerome, primary, Charrier, Celine, primary, Brion, Regis, primary, Lecanda, Fernando, primary, Verrecchia, Franck, primary, Heymann, Dominique, primary, Ellisen, Leif W., primary, and Ory, Benjamin, primary

Published
2023
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12. Data from Targeting the EWSR1-FLI1 Oncogene-Induced Protein Kinase PKC-β Abolishes Ewing Sarcoma Growth

Author

Surdez, Didier, primary, Benetkiewicz, Magdalena, primary, Perrin, Virginie, primary, Han, Zhi-Yan, primary, Pierron, Gaëlle, primary, Ballet, Stelly, primary, Lamoureux, François, primary, Rédini, Françoise, primary, Decouvelaere, Anne-Valérie, primary, Daudigeos-Dubus, Estelle, primary, Geoerger, Birgit, primary, de Pinieux, Gonzague, primary, Delattre, Olivier, primary, and Tirode, Franck, primary

Published
2023
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13. Supplementary Figure 1 from Targeting the EWSR1-FLI1 Oncogene-Induced Protein Kinase PKC-β Abolishes Ewing Sarcoma Growth

Author

Surdez, Didier, primary, Benetkiewicz, Magdalena, primary, Perrin, Virginie, primary, Han, Zhi-Yan, primary, Pierron, Gaëlle, primary, Ballet, Stelly, primary, Lamoureux, François, primary, Rédini, Françoise, primary, Decouvelaere, Anne-Valérie, primary, Daudigeos-Dubus, Estelle, primary, Geoerger, Birgit, primary, de Pinieux, Gonzague, primary, Delattre, Olivier, primary, and Tirode, Franck, primary

Published
2023
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14. Supplementary Figure 2 from Targeting the EWSR1-FLI1 Oncogene-Induced Protein Kinase PKC-β Abolishes Ewing Sarcoma Growth

Author

Surdez, Didier, primary, Benetkiewicz, Magdalena, primary, Perrin, Virginie, primary, Han, Zhi-Yan, primary, Pierron, Gaëlle, primary, Ballet, Stelly, primary, Lamoureux, François, primary, Rédini, Françoise, primary, Decouvelaere, Anne-Valérie, primary, Daudigeos-Dubus, Estelle, primary, Geoerger, Birgit, primary, de Pinieux, Gonzague, primary, Delattre, Olivier, primary, and Tirode, Franck, primary

Published
2023
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15. Data from Zoledronic Acid as a New Adjuvant Therapeutic Strategy for Ewing's Sarcoma Patients

Author

Odri, Guillaume A., primary, Dumoucel, Sophie, primary, Picarda, Gaëlle, primary, Battaglia, Séverine, primary, Lamoureux, François, primary, Corradini, Nadège, primary, Rousseau, Julie, primary, Tirode, Franck, primary, Laud, Karine, primary, Delattre, Olivier, primary, Gouin, François, primary, Heymann, Dominique, primary, and Redini, Françoise, primary

Published
2023
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16. Supplementary Table 1, Figures 1-3 from Zoledronic Acid as a New Adjuvant Therapeutic Strategy for Ewing's Sarcoma Patients

Author

Odri, Guillaume A., primary, Dumoucel, Sophie, primary, Picarda, Gaëlle, primary, Battaglia, Séverine, primary, Lamoureux, François, primary, Corradini, Nadège, primary, Rousseau, Julie, primary, Tirode, Franck, primary, Laud, Karine, primary, Delattre, Olivier, primary, Gouin, François, primary, Heymann, Dominique, primary, and Redini, Françoise, primary

Published
2023
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17. Supplementary Methods and Materials from Targeting the EWSR1-FLI1 Oncogene-Induced Protein Kinase PKC-β Abolishes Ewing Sarcoma Growth

Author

Surdez, Didier, primary, Benetkiewicz, Magdalena, primary, Perrin, Virginie, primary, Han, Zhi-Yan, primary, Pierron, Gaëlle, primary, Ballet, Stelly, primary, Lamoureux, François, primary, Rédini, Françoise, primary, Decouvelaere, Anne-Valérie, primary, Daudigeos-Dubus, Estelle, primary, Geoerger, Birgit, primary, de Pinieux, Gonzague, primary, Delattre, Olivier, primary, and Tirode, Franck, primary

Published
2023
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18. Supplementary Figure 4 from Targeting the EWSR1-FLI1 Oncogene-Induced Protein Kinase PKC-β Abolishes Ewing Sarcoma Growth

Author

Surdez, Didier, primary, Benetkiewicz, Magdalena, primary, Perrin, Virginie, primary, Han, Zhi-Yan, primary, Pierron, Gaëlle, primary, Ballet, Stelly, primary, Lamoureux, François, primary, Rédini, Françoise, primary, Decouvelaere, Anne-Valérie, primary, Daudigeos-Dubus, Estelle, primary, Geoerger, Birgit, primary, de Pinieux, Gonzague, primary, Delattre, Olivier, primary, and Tirode, Franck, primary

Published
2023
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19. Supplementary Tables 1-4 from Targeting the EWSR1-FLI1 Oncogene-Induced Protein Kinase PKC-β Abolishes Ewing Sarcoma Growth

Author

Surdez, Didier, primary, Benetkiewicz, Magdalena, primary, Perrin, Virginie, primary, Han, Zhi-Yan, primary, Pierron, Gaëlle, primary, Ballet, Stelly, primary, Lamoureux, François, primary, Rédini, Françoise, primary, Decouvelaere, Anne-Valérie, primary, Daudigeos-Dubus, Estelle, primary, Geoerger, Birgit, primary, de Pinieux, Gonzague, primary, Delattre, Olivier, primary, and Tirode, Franck, primary

Published
2023
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20. Data from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis

Author

Rodriguez Calleja, Lidia, primary, Jacques, Camille, primary, Lamoureux, François, primary, Baud'huin, Marc, primary, Tellez Gabriel, Marta, primary, Quillard, Thibaut, primary, Sahay, Debashish, primary, Perrot, Pierre, primary, Amiaud, Jerome, primary, Charrier, Celine, primary, Brion, Regis, primary, Lecanda, Fernando, primary, Verrecchia, Franck, primary, Heymann, Dominique, primary, Ellisen, Leif W., primary, and Ory, Benjamin, primary

Published
2023
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21. Supplementary Figure Legends from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis

Author

Rodriguez Calleja, Lidia, primary, Jacques, Camille, primary, Lamoureux, François, primary, Baud'huin, Marc, primary, Tellez Gabriel, Marta, primary, Quillard, Thibaut, primary, Sahay, Debashish, primary, Perrot, Pierre, primary, Amiaud, Jerome, primary, Charrier, Celine, primary, Brion, Regis, primary, Lecanda, Fernando, primary, Verrecchia, Franck, primary, Heymann, Dominique, primary, Ellisen, Leif W., primary, and Ory, Benjamin, primary

Published
2023
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22. Supplementary Figure 6 from Targeting the EWSR1-FLI1 Oncogene-Induced Protein Kinase PKC-β Abolishes Ewing Sarcoma Growth

Author

Surdez, Didier, primary, Benetkiewicz, Magdalena, primary, Perrin, Virginie, primary, Han, Zhi-Yan, primary, Pierron, Gaëlle, primary, Ballet, Stelly, primary, Lamoureux, François, primary, Rédini, Françoise, primary, Decouvelaere, Anne-Valérie, primary, Daudigeos-Dubus, Estelle, primary, Geoerger, Birgit, primary, de Pinieux, Gonzague, primary, Delattre, Olivier, primary, and Tirode, Franck, primary

Published
2023
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23. Supplementary Figure 5 from Targeting the EWSR1-FLI1 Oncogene-Induced Protein Kinase PKC-β Abolishes Ewing Sarcoma Growth

Author

Surdez, Didier, primary, Benetkiewicz, Magdalena, primary, Perrin, Virginie, primary, Han, Zhi-Yan, primary, Pierron, Gaëlle, primary, Ballet, Stelly, primary, Lamoureux, François, primary, Rédini, Françoise, primary, Decouvelaere, Anne-Valérie, primary, Daudigeos-Dubus, Estelle, primary, Geoerger, Birgit, primary, de Pinieux, Gonzague, primary, Delattre, Olivier, primary, and Tirode, Franck, primary

Published
2023
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24. Supplementary Figure 7 from Targeting the EWSR1-FLI1 Oncogene-Induced Protein Kinase PKC-β Abolishes Ewing Sarcoma Growth

Author

Surdez, Didier, primary, Benetkiewicz, Magdalena, primary, Perrin, Virginie, primary, Han, Zhi-Yan, primary, Pierron, Gaëlle, primary, Ballet, Stelly, primary, Lamoureux, François, primary, Rédini, Françoise, primary, Decouvelaere, Anne-Valérie, primary, Daudigeos-Dubus, Estelle, primary, Geoerger, Birgit, primary, de Pinieux, Gonzague, primary, Delattre, Olivier, primary, and Tirode, Franck, primary

Published
2023
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25. Supplementary Figure 3 from Targeting the EWSR1-FLI1 Oncogene-Induced Protein Kinase PKC-β Abolishes Ewing Sarcoma Growth

Author

Surdez, Didier, primary, Benetkiewicz, Magdalena, primary, Perrin, Virginie, primary, Han, Zhi-Yan, primary, Pierron, Gaëlle, primary, Ballet, Stelly, primary, Lamoureux, François, primary, Rédini, Françoise, primary, Decouvelaere, Anne-Valérie, primary, Daudigeos-Dubus, Estelle, primary, Geoerger, Birgit, primary, de Pinieux, Gonzague, primary, Delattre, Olivier, primary, and Tirode, Franck, primary

Published
2023
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26. Chimeric protein EWS::FLI1 drives cell proliferation in Ewing Sarcoma viaaberrant expression of KCNN1/SK1 and dysregulation of calcium signaling

Author

Dupuy, Maryne, Gueguinou, Maxime, Postec, Anaïs, Brion, Régis, Tesfaye, Robel, Mullard, Mathilde, Regnier, Laura, Amiaud, Jérôme, Hubsch, Clémence, Potier-Cartereau, Marie, Chantôme, Aurélie, Brounais-Le Royer, Bénédicte, Baud’huin, Marc, Georges, Steven, Lamoureux, François, Ory, Benjamin, Entz-Werlé, Natacha, Delattre, Olivier, Rédini, Françoise, Vandier, Christophe, and Verrecchia, Franck

Abstract

Ewing sarcoma (ES) is characterized by EWS::FLI1 or EWS::ERG fusion proteins. Knowing that ion channels are involved in tumorigenesis, this work aimed to study the involvement of the KCNN1gene, which encodes the SK1 potassium channel, in ES development. Bioinformatics analyses from databases were used to study KCNN1expression in patients and cell lines. Molecular approaches and in vitro assays were used to study the transcriptional regulation of KCNN1and its involvement in the regulation of ES cell proliferation. KCNN1is overexpressed in ES patient biopsies, and its expression is inversely correlated with patient survival. EWS::FLI1, like EWS::ERG, promotes KCNN1and SK1 expression, binding to GGAA microsatellites near the promoter of KCNN1isoforms. KCNN1is involved in the regulation of ES cell proliferation, with its silencing being associated with a slowing of the cell cycle, and its expression modulates membrane potential and therefore calcium flux. These results highlight that KCNN1is a direct target of EWS::FLI1 and EWS::ERG and demonstrate that KCNN1is involved in the regulation of intracellular calcium activity and ES cell proliferation, making it a promising therapeutic target in ES.

Published
2024
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29. Editorial: Developing next-generation therapeutics to defeat mutation-driven cancer.

Author

Chow, Frances, Lamoureux, François, and Moriceau, Gatien

Subjects
T-cell exhaustion, THERAPEUTICS, NON-small-cell lung carcinoma, AP-1 transcription factor, COMBINATION drug therapy
Abstract

The editorial in Frontiers in Immunology discusses the challenges posed by mutation-driven cancers and the need for innovative therapeutic strategies to combat them. The research topic focuses on preclinical studies, target-based mechanisms for combination therapies, and approaches to overcome resistance to current treatments. The editorial highlights a study on predicting pancreatic cancer prognosis based on KRAS mutation status, as well as reviews on the potential of antibody-drug conjugates for lung cancer and FGFR-targeting therapies for urothelial carcinoma. The authors emphasize the importance of ongoing research in developing next-generation therapeutics to address mutation-driven cancers. [Extracted from the article]

Published
2024
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30. Abstract 3902: TRIM33 interacts with HSF1 in osteosarcoma development

Author

Lallier, Morgane, primary, Tefaye, Robel, additional, Moukengué, Brice, additional, Charrier, Céline, additional, Thepault, Rose-Anne, additional, Royer, Benedicte Brounais-Le, additional, Baud'huin, Marc, additional, Verrecchia, Franck, additional, Ory, Benjamin, additional, and Lamoureux, François, additional

Published
2022
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32. Abstract 6325: Identification of genes responsible for osteosarcomas metastatic evolution by active super enhancers profiling

Author

Lavaud, Mélanie, primary, Tesfaye, Robel, additional, Charrier, Céline, additional, Thépault, Rose Anne, additional, Golias, Maxime, additional, Page, Sarah Le, additional, Mullard, Mathilde, additional, Brounais, Bénédicte, additional, Verrecchia, Franck, additional, Baud'huin, Marc, additional, Lamoureux, François, additional, Georges, Steven, additional, and Ory, Benjamin, additional

Published
2022
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36. Molecular Chaperones in Osteosarcoma: Diagnosis and Therapeutic Issues

Author

Lallier, Morgane, Marchandet, Louise, Moukengue, Brice, Charrier, Celine, Baud’huin, Marc, Verrecchia, Franck, Ory, Benjamin, and Lamoureux, François

Subjects
endocrine system, Carcinogenesis, HSPs, Bone Neoplasms, Review, bone tumor, HSF1, Models, Biological, lcsh:Biology (General), osteosarcoma, Animals, Humans, lcsh:QH301-705.5, Heat-Shock Proteins, Molecular Chaperones
Abstract

Osteosarcoma (OS) is the most common form of primary bone tumor affecting mainly children and young adults. Despite therapeutic progress, the 5-year survival rate is 70%, but it drops drastically to 30% for poor responders to therapies or for patients with metastases. Identifying new therapeutic targets is thus essential. Heat Shock Proteins (HSPs) are the main effectors of Heat Shock Response (HSR), the expression of which is induced by stressors. HSPs are a large family of proteins involved in the folding and maturation of other proteins in order to maintain proteostasis. HSP overexpression is observed in many cancers, including breast, prostate, colorectal, lung, and ovarian, as well as OS. In this article we reviewed the significant role played by HSPs in molecular mechanisms leading to OS development and progression. HSPs are directly involved in OS cell proliferation, apoptosis inhibition, migration, and drug resistance. We focused on HSP27, HSP60, HSP70 and HSP90 and summarized their potential clinical uses in OS as either biomarkers for diagnosis or therapeutic targets. Finally, based on different types of cancer, we consider the advantage of targeting heat shock factor 1 (HSF1), the major transcriptional regulator of HSPs in OS.

Published
2021

37. Overexpression of the Ubiquitin Specific Proteases USP43, USP41, USP27x and USP6 in Osteosarcoma Cell Lines: Inhibition of Osteosarcoma Tumor Growth and Lung Metastasis Development by the USP Antagonist PR619

Author

Lavaud, Mélanie, primary, Mullard, Mathilde, additional, Tesfaye, Robel, additional, Amiaud, Jérôme, additional, Legrand, Mélanie, additional, Danieau, Geoffroy, additional, Brion, Régis, additional, Morice, Sarah, additional, Regnier, Laura, additional, Dupuy, Maryne, additional, Brounais-Le Royer, Bénédicte, additional, Lamoureux, François, additional, Ory, Benjamin, additional, Rédini, Françoise, additional, and Verrecchia, Franck, additional

Published
2021
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38. Ribosomopathies: New Therapeutic Perspectives

Author

Orgebin, Emilien, Lamoureux, François, Isidor, Bertrand, Charrier, Céline, Ory, Benjamin, Lézot, Frédéric, Baud’huin, Marc, BAUD'HUIN, Marc, Sarcomes osseux et remodelage des tissus calcifiés - Phy-Os [Nantes - INSERM U1238] (Phy-Os), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Bretagne Loire (UBL)-Centre hospitalier universitaire de Nantes (CHU Nantes), Centre hospitalier universitaire de Nantes (CHU Nantes), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Bretagne Loire (UBL)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), and Université de Nantes (UN)-Université de Nantes (UN)

Subjects
Ribosomal Proteins, riboprotein, treatment, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Review, [SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics, lcsh:Biology (General), [SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics, ribosome, Humans, lcsh:QH301-705.5, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, Ribosomes, ComputingMilieux_MISCELLANEOUS, ribosomopathies, Anemia, Diamond-Blackfan
Abstract

Ribosomopathies are a group of rare diseases in which genetic mutations cause defects in either ribosome biogenesis or function, given specific phenotypes. Ribosomal proteins, and multiple other factors that are necessary for ribosome biogenesis (rRNA processing, assembly of subunits, export to cytoplasm), can be affected in ribosomopathies. Despite the need for ribosomes in all cell types, these diseases result mainly in tissue-specific impairments. Depending on the type of ribosomopathy and its pathogenicity, there are many potential therapeutic targets. The present manuscript will review our knowledge of ribosomopathies, discuss current treatments, and introduce the new therapeutic perspectives based on recent research. Diamond–Blackfan anemia, currently treated with blood transfusion prior to steroids, could be managed with a range of new compounds, acting mainly on anemia, such as L-leucine. Treacher Collins syndrome could be managed by various treatments, but it has recently been shown that proteasomal inhibition by MG132 or Bortezomib may improve cranial skeleton malformations. Developmental defects resulting from ribosomopathies could be also treated pharmacologically after birth. It might thus be possible to treat certain ribosomopathies without using multiple treatments such as surgery and transplants. Ribosomopathies remain an open field in the search for new therapeutic approaches based on our recent understanding of the role of ribosomes and progress in gene therapy for curing genetic disorders.

Published
2020

39. Implication of the p53-Related miR-34c, -125b, and -203 in the Osteoblastic Differentiation and the Malignant Transformation of Bone Sarcomas

Author

Jacques, Camille, Tesfaye, Robel, Lavaud, Melanie, Georges, Steven, Baud'Huin, Marc, Lamoureux, François, Ory, Benjamin, Baud’huin, Marc, Equipe Labellisée LIGUE 2012 [Nantes], Sarcomes osseux et remodelage des tissus calcifiés - Phy-Os [Nantes - INSERM U1238] (Phy-Os), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Bretagne Loire (UBL)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Physiopathologie des Adaptations Nutritionnelles (PhAN), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Physiopathologie de la résorption osseuse et thérapie des tumeurs osseuses primitives, and Université de Nantes (UN)-IFR26-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
musculoskeletal diseases, Osteoblasts, [SDV]Life Sciences [q-bio], Bone Neoplasms, Cell Differentiation, Review, bone, microRNAs, Cell Transformation, Neoplastic, lcsh:Biology (General), osteosarcoma, Animals, Humans, Tumor Suppressor Protein p53, lcsh:QH301-705.5
Abstract

International audience; The formation of the skeleton occurs throughout the lives of vertebrates and is achieved through the balanced activities of two kinds of specialized bone cells: the bone-forming osteoblasts and the bone-resorbing osteoclasts. Impairment in the remodeling processes dramatically hampers the proper healing of fractures and can also result in malignant bone diseases such as osteosarcoma. MicroRNAs (miRNAs) are a class of small non-coding single-strand RNAs implicated in the control of various cellular activities such as proliferation, differentiation, and apoptosis. Their post-transcriptional regulatory role confers on them inhibitory functions toward specific target mRNAs. As miRNAs are involved in the differentiation program of precursor cells, it is now well established that this class of molecules also influences bone formation by affecting osteoblastic differentiation and the fate of osteoblasts. In response to various cell signals, the tumor-suppressor protein p53 activates a huge range of genes, whose miRNAs promote genomic-integrity maintenance, cell-cycle arrest, cell senescence, and apoptosis. Here, we review the role of three p53-related miRNAs, miR-34c, -125b, and -203, in the bone-remodeling context and, in particular, in osteoblastic differentiation. The second aim of this study is to deal with the potential implication of these miRNAs in osteosarcoma development and progression.

Published
2020

40. TH1579, MTH1 inhibitor, delays tumour growth and inhibits metastases 1 development in osteosarcoma model 2 3

Author

Moukengue, Brice, Brown, Hannah, Charrier, Eline, Battaglia, Everine, Baud'Huin, Marc, Quillard, Thibaut, Pham, Therese, Pateras, Ioannis, Gorgoulis, Vassilis, Helleday, Thomas, Heymann, Dominique, Warpman Berglund, Ulrika, Ory, Benjamin, Lamoureux, François, Sarcomes osseux et remodelage des tissus calcifiés - Phy-Os [Nantes - INSERM U1238] (Phy-Os), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Bretagne Loire (UBL)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Department of Oncology and Metabolism [Sheffield, UK] (European Associated Laboratory 'Sarcoma Research Unit'), The University of Sheffield [Sheffield, U.K.], Department of Oncology and Metabolism [Sheffield, UK], Cancer Center Karolinska [Karolinska Institutet] (CCK), Karolinska Institutet [Stockholm], National and Kapodistrian University of Athens (NKUA), Physiopathologie des Adaptations Nutritionnelles (PhAN), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Department of Oncology and Metabolism [Sheffield, UK] (INSERM European Associated Laboratory 'Sarcoma Research Unit'), and maurice, sandrine

Subjects
Osteosarcoma, [SDV.CAN] Life Sciences [q-bio]/Cancer, DNA damage, ROS, [SDV.CAN]Life Sciences [q-bio]/Cancer, Bone tumours, MTH1
Abstract

International audience; Background: Osteosarcoma (OS) is the most common primary malignant bone tumour. Unfortunately, no new treatments are approved and over the last 30 years the survival rate remains only 30% at 5 years for poor res-ponders justifying an urgent need of new therapies. The Mutt homolog 1 (MTH1) enzyme prevents incorporation of oxidized nucleotides into DNA and recently developed MTH1 inhibitors may offer therapeutic potential as MTH1 is overexpressed in various cancers. Methods: The aim of this study was to evaluate the therapeutic benefits of targeting MTH1 with two chemical inhibitors, TH588 and TH1579 on human osteosarcoma cells. Preclinical efficacy of TH1579 was assessed in human osteosarcoma xenograft model on tumour growth and development of pulmonary metastases. Findings: MTH1 is overexpressed in OS patients and tumour cell lines, compared to mesenchymal stem cells. In vitro, chemical inhibition of MTH1 by TH588 and TH1579 decreases OS cells viability, impairs their cell cycle and increases apoptosis in OS cells. TH1579 was confirmed to bind MTH1 by CETSA in OS model. Moreover , 90 mg/kg of TH1579 reduces in vivo tumour growth by 80.5% compared to non-treated group at day 48. This result was associated with the increase in 8-oxo-dG integration into tumour cells DNA and the increase of apoptosis. Additionally, TH1579 also reduces the number of pulmonary metastases. Interpretation: All these results strongly provide a pre-clinical proof-of-principle that TH1579 could be a therapeutic option for patients with osteosarcoma. Funding: This study was supported by La Ligue Contre le Cancer, la SFCE and Enfants Cancers Sant e.

Published
2020

41. BET bromodomains' functions in bone-related pathologies

Author

Jacques, Camille, Lavaud, Melanie, Georges, Steven, Tesfaye, Robel, Baud'Huin, Marc, Lamoureux, François, Ory, Benjamin, Baud’huin, Marc, Equipe Labellisée LIGUE 2012 [Nantes], Sarcomes osseux et remodelage des tissus calcifiés - Phy-Os [Nantes - INSERM U1238] (Phy-Os), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Bretagne Loire (UBL)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Physiopathologie des Adaptations Nutritionnelles (PhAN), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), and Université de Nantes (UN)-Université de Nantes (UN)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)

Subjects
Cancer Research, BRD4, JQ1, [SDV]Life Sciences [q-bio], Osteoporosis, Context (language use), Bone Neoplasms, Sarcoma, Ewing, Biology, Bioinformatics, I-BET, bone, Epigenesis, Genetic, Histones, 03 medical and health sciences, 0302 clinical medicine, Protein Domains, Genetics, medicine, Humans, Epigenetics, 030304 developmental biology, BET bromodomains, 0303 health sciences, chondrosarcoma, Osteosarcoma, Mechanism (biology), Proteins, Acetylation, medicine.disease, Bromodomain, Primary bone, 030220 oncology & carcinogenesis, Protein Processing, Post-Translational, Ewing sarcoma, epigenetic
Abstract

International audience; Throughout life, bones are subjected to the so-called 'bone-remodeling' process, which is a balanced mechanism between the apposition and the resorption of bone. This remodeling process depends on the activities of bone-specialized cells, namely the osteoblasts and the osteoclasts. Any deregulation in this process results in bone-related pathologies, classified as either metabolic nonmalignant diseases (such as osteoporosis) or malignant primary bone sarcomas. As these pathologies are not characterized by common targetable genetic alterations, epigenetic strategies could be relevant and promising options. Recently, targeting epigenetic regulators such as the bromodomains and extraterminal domains (BET) readers have achieved success in numerous other pathologies, including cancers. In this review, we highlight the current state of the art in terms of the diverse implications of BET bromodomain proteins in the bone's biology and its defects. Consequently, their role in bone-related pathologies will also be developed, especially in the context of the primary bone sarcomas.

Published
2019

44. List of Contributors

Author

Ando, Kosei, primary, Arslandemir, Coskun, additional, Bell, Walter C., additional, Berdal, Ariane, additional, Berthold, Dominik, additional, Bhat, Bheem M., additional, Bhat, Ramesh A., additional, Bhattacharyya, Sudeepa, additional, Billiard, Julia, additional, Blanchard, Frederic, additional, Bodine, Peter V.N., additional, Böhling, Tom, additional, Bouattour, Aymann, additional, Bouvier, Corinne, additional, Brounais, Bénédicte, additional, Brunetti, Giacomina, additional, Byrum, Stephanie, additional, Chappard, Daniel, additional, Chow, Edward, additional, Clezardin, Philippe, additional, Clines, Gregory A., additional, Clohisy, Denis R., additional, Colucci, Silvia, additional, David, Emmanuelle, additional, Pinieux, Gonzague de, additional, Descroix, Vianney, additional, DeDosso, Sara, additional, Dougall, William C., additional, Dunn, Lauren K., additional, Fairchild, Alysa, additional, Ferrari, Stefano, additional, Filgueira, Luis, additional, Flanagan, Adrienne M., additional, Fortun, Yannick, additional, Fournier, Pierrick, additional, Ghoul-Mazgar, Sonia, additional, Gikas, Panagiotis D., additional, Gosheger, Georg, additional, Gouin, François, additional, Grano, Maria, additional, Guise, Theresa A., additional, Hardes, Jendrik, additional, Hauben, Esther I., additional, Heffernan, Eric J., additional, Herrera, Monica, additional, Herrera, Fernanda G., additional, Heymann, Dominique, additional, Hicks, David G., additional, Hird, Amanda, additional, Hogendoorn, Pancras C.W., additional, Holen, Ingunn, additional, Jimenez-Andrade, Juan Miguel, additional, Jones, Robert G., additional, Khoury, Joseph, additional, Knuutila, Sakari, additional, Kontny, Udo, additional, Lamoureux, François, additional, Lau, Ching C., additional, Lawrentschuk, Nathan, additional, Lawson, Michelle A., additional, Lee, Jiyun, additional, Lezot, Frederic, additional, Li, Shibo, additional, Loberg, Robert D., additional, Man, Tsz-Kwong, additional, Mantyh, Patrick W., additional, Martin, Mallory, additional, Matsusue, Yoshitaka, additional, Mercuri, Mario, additional, Mori, Kanji, additional, Munk, Peter L., additional, Murrills, Richard J., additional, Padrines, Marc, additional, Palmerini, Emanuela, additional, Park, Paul C., additional, Paterson, Alexander HG, additional, Picarda, Gaëlle, additional, Pienta, Kenneth J., additional, Rajarubendra, Nieroshan, additional, Rao, Pulivarthi H., additional, Rashid, Faisal, additional, Rédini, Françoise, additional, Richards, Carl D., additional, Robinson, John A., additional, Rousseau, Julie, additional, Ruhin, Blandine, additional, Ruiz, Velasco C., additional, Sabino, Ma’Ann C., additional, Savola, Suvi, additional, Schirrmeister, Holger, additional, Seibel, Markus J., additional, Selvarajah, Shamini, additional, Siegal, Gene P., additional, Siegel, Eric R., additional, Smyth, David, additional, Squire, Jeremy A., additional, Staals, Eric L., additional, Steitbueger, Arne, additional, Suva, Larry J., additional, Tang, Ping, additional, Tirabosco, Roberto, additional, Trichet, Valérie, additional, Vardanyan, Marina, additional, and Zielenska, Maria, additional

Published
2010
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45. Sonic Hedgehog Signature in Pediatric Primary Bone Tumors: Effects of the GLI Antagonist GANT61 on Ewing’s Sarcoma Tumor Growth

Author

Mullard, Mathilde, primary, Cadé, Marie, additional, Morice, Sarah, additional, Dupuy, Maryne, additional, Danieau, Geoffroy, additional, Amiaud, Jérome, additional, Renault, Sarah, additional, Lézot, Frédéric, additional, Brion, Régis, additional, Thepault, Rose Anne, additional, Ory, Benjamin, additional, Lamoureux, François, additional, Corre, Isabelle, additional, Brounais-LeRoyer, Bénédicte, additional, Rédini, Françoise, additional, and Verrecchia, Franck, additional

Published
2020
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49. Implication of molecular vascular smooth muscle cell heterogeneity among arterial beds in arterial calcification

Author

Espitia, Olivier, Chatelais, Mathias, Steenman, Marja, Charrier, Céline, Maurel, Blandine, Georges, Steven, Houlgatte, Rémi, Verrecchia, Franck, Ory, Benjamin, Lamoureux, François, Heymann, Dominique, Gouëffic, Yann, Quillard, Thibaut, Sarcomes osseux et remodelage des tissus calcifiés - Phy-Os [Nantes - INSERM U1238] (Phy-Os), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Bretagne Loire (UBL)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Hôtel-Dieu de Nantes, Unité de recherche de l'institut du thorax (ITX-lab), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Nutrition-Génétique et Exposition aux Risques Environnementaux (NGERE), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL), Délégation à la Recherche Clinique et à l'Innovation [CHRU Nancy] (DRCI), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Institut de Cancérologie de l'Ouest [Angers/Nantes] (UNICANCER/ICO), UNICANCER, Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN), Department of Oncology and Metabolism [Sheffield, UK] (INSERM European Associated Laboratory 'Sarcoma Research Unit'), The University of Sheffield [Sheffield, U.K.], Centre de Recherche en Cancérologie et Immunologie Nantes-Angers (CRCINA), Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes), Programme Hospitalier de Recherche Clinique (PROG/11/58) to YG. The Fondation de l'Avenir pour la Recherche Médicale Appliquée (ET4-720, http://www.fondationdelavenir.org/) to TQ, the Centre Hospitalier Universitaire de Nantes to TQ, and the Agence Nationale de la Recherche (ANR-16-CE14-0012-01, www.agence-nationale-recherche.fr) to BO. Thibaut Quillard's salary has been provided by the Fondation Lefoulon Delalande (http://lefoulon-delalande.institut-de-france.fr/), the European commission (FP7 People: Marie-Curie Actions, grant 627418, https://ec.europa.eu/research/mariecurieactions/), and the Centre Hospitalier Universitaire de Nantes. Steven George's salary has been provided by the Agence Nationale de la Recherche (ANR-16-CE14-0012-01, www.agence-nationale-recherche.fr)., ANR-16-CE14-0012,EPIBONE,Rôle des protéines à bromodomaines dans la physiologie osseuse normale(2016), European Project: 627418,EC:FP7:PEOPLE,FP7-PEOPLE-2013-IIF,CALTHERO(2014), maurice, sandrine, Comparative Study And Mechanisms Of Calcification Heterogeneity In Atherosclerotic Plaques - CALTHERO - - EC:FP7:PEOPLE2014-07-01 - 2016-06-30 - 627418 - VALID, Hôpital Hôtel-Dieu [Nantes] (Centre Hospitalier Universitaire de Nantes), unité de recherche de l'institut du thorax UMR1087 UMR6291 (ITX), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA), and Université de Nantes (UN)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Cell biology, Cell signaling, Physiology, Immune Cells, Immunology, lcsh:Medicine, Signal transduction, Muscle, Smooth, Vascular, Calcification, White Blood Cells, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Animal Cells, Medicine and Health Sciences, Genetics, Humans, lcsh:Science, Aorta, Cells, Cultured, [SDV.MHEP.RSOA] Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system, Blood Cells, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Macrophages, lcsh:R, Biology and Life Sciences, Signaling cascades, Computational Biology, Calcinosis, Cell Differentiation, Arteries, Genomics, Femoral Arteries, Genome Analysis, Plaque, Atherosclerotic, [SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Carotid Arteries, TGF-beta signaling cascade, [SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system, Cardiovascular Anatomy, Blood Vessels, lcsh:Q, Anatomy, Cellular Types, Physiological Processes, Transcriptome, Transcriptome Analysis, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Research Article
Abstract

International audience; Vascular calcification is a strong and independent predictive factor for cardiovascular complications and mortality. Our previous work identified important discrepancies in plaque composition and calcification types between carotid and femoral arteries. The objective of this study is to further characterize and understand the heterogeneity in vascular calcifica-tion among vascular beds, and to identify molecular mechanisms underlying this process. We established ECLAGEN biocollection that encompasses human atherosclerotic lesions and healthy arteries from different locations (abdominal, thoracic aorta, carotid, femoral, and infrapopliteal arteries) for histological, cell isolation, and transcriptomic analysis. Our results show that lesion composition differs between these locations. Femoral arteries are the most calcified arteries overall. They develop denser calcifications (sheet-like, nodule), and are highly susceptible to osteoid metaplasia. These discrepancies may derive from intrinsic differences between SMCs originating from these locations, as microarray analysis showed specific transcriptomic profiles between primary SMCs isolated from each arterial bed. These molecular differences translated into functional disparities. SMC from femoral arteries showed the highest propensity to mineralize due to an increase in basal TGFβ sig-naling. Our results suggest that biological heterogeneity of resident vascular cells between arterial beds, reflected by our transcriptomic analysis, is critical in understanding plaque biology and calcification, and may have strong implications in vascular therapeutic approaches.

Published
2018

50. RPL13 Variants Cause Spondyloepimetaphyseal Dysplasia with Severe Short Stature

Author

Le Caignec, Cedric, primary, Ory, Benjamin, additional, Lamoureux, François, additional, O’Donohue, Marie-Francoise, additional, Orgebin, Emilien, additional, Lindenbaum, Pierre, additional, Téletchéa, Stéphane, additional, Saby, Manon, additional, Hurst, Anna, additional, Nelson, Katherine, additional, Gilbert, Shawn R., additional, Wilnai, Yael, additional, Zeitlin, Leonid, additional, Segev, Eitan, additional, Tesfaye, Robel, additional, Nizon, Mathilde, additional, Cogne, Benjamin, additional, Bezieau, Stéphane, additional, Geoffroy, Loic, additional, Hamel, Antoine, additional, Mayrargue, Emmanuelle, additional, de Courtivron, Benoît, additional, Decock-Giraudaud, Aliette, additional, Charrier, Céline, additional, Pichon, Olivier, additional, Retière, Christelle, additional, Redon, Richard, additional, Pepler, Alexander, additional, McWalter, Kirsty, additional, Da Costa, Lydie, additional, Toutain, Annick, additional, Gleizes, Pierre-Emmanuel, additional, Baud’huin, Marc, additional, and Isidor, Bertrand, additional

Published
2019
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