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1. 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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2. 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., Lavaud, Melanie, Charrier, Celine, Brounais-Le Royer, Benedicte, Cartron, Pierre-Francois, Verrecchia, Franck, Baud'huin, Marc, Lamoureux, Francois, Georges, Steven, and Ory, Benjamin

Subjects
Herbicides -- Environmental aspects -- Health aspects -- Genetic aspects, Osteoblasts -- Physiological aspects -- Health aspects, Osteoclasts (Biology) -- Physiological aspects -- Health aspects, Cell differentiation -- Genetic aspects -- Health aspects, Environmental issues, Health
Abstract

Background: Osteoclasts are major actors in the maintenance of bone homeostasis. The full functional maturation of osteoclasts from monocyte lineage cells is essential for the degradation of old/damaged bone matrix. Diuron is one of the most frequently encountered herbicides, particularly in water sources. However, despite a reported delayed ossification in vivo, its impact on bone cells remains largely unknown. Objectives: The objectives of this study were to first better characterize osteoclastogenesis by identifying genes that drive the differentiation of [CD14.sup.+] monocyte progenitors into osteoclasts and to evaluate the toxicity of diuron on osteoblastic and osteoclastic differentiation in vitro. Methods: We performed chromatin immunoprecipitation (ChIP) against H3K27ac followed by ChIP-sequencing (ChIP-Seq) and RNA-sequencing (RNA-Seq) at different stages of differentiation of [CD14.sup.+] monocytes into active osteoclasts. Differentially activated super-enhancers and their potential target genes were identified. Then to evaluate the toxicity of diuron on osteoblasts and osteoclasts, we performed RNA-Seq and functional tests during in vitro osteoblastic and osteoclastic differentiation by exposing cells to different concentrations of diuron. RESULTS: The combinatorial study of the epigenetic and transcriptional remodeling taking place during differentiation has revealed a very dynamic epigenetic profile that supports the expression of genes vital for osteoclast differentiation and function. In total, we identified 122 genes induced by dynamic super-enhancers at late days. Our data suggest that high concentration of diuron (50 [micro]M) affects viability of mesenchymal stem cells (MSCs) in vitro associated with a decrease of bone mineralization. At a lower concentration (1 [micro]M), an inhibitory effect was observed in vitro on the number of osteoclasts derived from [CD14.sup.+] monocytes without affecting cell viability. Among the diuron-affected genes, our analysis suggests a significant enrichment of genes targeted by pro-differentiation super-enhancers, with an odds ratio of 5.12 (p = 2.59 * [10.sup.-5]). DISCUSSION: Exposure to high concentrations of diuron decreased the viability of MSCs and could therefore affect osteoblastic differentiation and bone mineralization. This pesticide also disrupted osteoclasts maturation by impairing the expression of cell-identity determining genes. Indeed, at sublethal concentrations, differences in the expression of these key genes were mild during the course of in vitro osteoclast differentiation. Taken together our results suggest that high exposure levels of diuron could have an effect on bone homeostasis. https://doi.org/10.1289/EHP11690, Introduction Bone tissue is maintained through continual bone remodeling during the life of an individual. This process involves mainly two cell types: the osteoblasts and the osteoclasts, respectively producing and [...]

Published
2023
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5. Biological Sample Collection to Advance Research and Treatment: A Fight Osteosarcoma Through European Research and Euro Ewing Consortium Statement

Author

Onderzoek Beeld, Green, Darrell, van Ewijk, Roelof, Tirtei, Elisa, Andreou, Dimosthenis, Baecklund, Fredrik, Baumhoer, Daniel, Bielack, Stefan S., Botchu, Rajesh, Boye, Kjetil, Brennan, Bernadette, Capra, Michael, Cottone, Lucia, Dirksen, Uta, Fagioli, Franca, Fernandez, Natalia, Flanagan, Adrienne M., Gambarotti, Marco, Gaspar, Nathalie, Gelderblom, Hans, Gerrand, Craig, Gomez-Mascard, Anne, Hardes, Jendrik, Hecker-Nolting, Stefanie, Kabickova, Edita, Kager, Leo, Kanerva, Jukka, Kester, Lennart A., Kuijjer, Marieke L., Laurence, Valérie, Lervat, Cyril, Marchais, Antonin, Marec-Berard, Perrine, Mendes, Cristina, Merks, Johannes H.M., Ory, Benjamin, Palmerini, Emanuela, Pantziarka, Pan, Papakonstantinou, Evgenia, Piperno-Neumann, Sophie, Raciborska, Anna, Roundhill, Elizabeth A., Rutkauskaite, Vilma, Safwat, Akmal, Scotlandi, Katia, Staals, Eric L., Strauss, Sandra J., Surdez, Didier, Sys, Gwen M.L., Tabone, Marie Dominique, Toulmonde, Maud, Valverde, Claudia, van de Sande, Michiel A.J., Wörtler, Klaus, Campbell-Hewson, Quentin, McCabe, Martin G., Nathrath, Michaela, Onderzoek Beeld, Green, Darrell, van Ewijk, Roelof, Tirtei, Elisa, Andreou, Dimosthenis, Baecklund, Fredrik, Baumhoer, Daniel, Bielack, Stefan S., Botchu, Rajesh, Boye, Kjetil, Brennan, Bernadette, Capra, Michael, Cottone, Lucia, Dirksen, Uta, Fagioli, Franca, Fernandez, Natalia, Flanagan, Adrienne M., Gambarotti, Marco, Gaspar, Nathalie, Gelderblom, Hans, Gerrand, Craig, Gomez-Mascard, Anne, Hardes, Jendrik, Hecker-Nolting, Stefanie, Kabickova, Edita, Kager, Leo, Kanerva, Jukka, Kester, Lennart A., Kuijjer, Marieke L., Laurence, Valérie, Lervat, Cyril, Marchais, Antonin, Marec-Berard, Perrine, Mendes, Cristina, Merks, Johannes H.M., Ory, Benjamin, Palmerini, Emanuela, Pantziarka, Pan, Papakonstantinou, Evgenia, Piperno-Neumann, Sophie, Raciborska, Anna, Roundhill, Elizabeth A., Rutkauskaite, Vilma, Safwat, Akmal, Scotlandi, Katia, Staals, Eric L., Strauss, Sandra J., Surdez, Didier, Sys, Gwen M.L., Tabone, Marie Dominique, Toulmonde, Maud, Valverde, Claudia, van de Sande, Michiel A.J., Wörtler, Klaus, Campbell-Hewson, Quentin, McCabe, Martin G., and Nathrath, Michaela

Published
2024

10. 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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13. Sarcoma treatment in the era of molecular medicine

Author

Grünewald, Thomas GP, Alonso, Marta, Avnet, Sofia, Banito, Ana, Burdach, Stefan, Cidre‐Aranaz, Florencia, Di Pompo, Gemma, Distel, Martin, Dorado‐Garcia, Heathcliff, Garcia‐Castro, Javier, González‐González, Laura, Grigoriadis, Agamemnon E, Kasan, Merve, Koelsche, Christian, Krumbholz, Manuela, Lecanda, Fernando, Lemma, Silvia, Longo, Dario L, Madrigal‐Esquivel, Claudia, Morales‐Molina, Álvaro, Musa, Julian, Ohmura, Shunya, Ory, Benjamin, Pereira‐Silva, Miguel, Perut, Francesca, Rodriguez, Rene, Seeling, Carolin, Al Shaaili, Nada, Shaabani, Shabnam, Shiavone, Kristina, Sinha, Snehadri, Tomazou, Eleni M, Trautmann, Marcel, Vela, Maria, Versleijen‐Jonkers, Yvonne MH, Visgauss, Julia, Zalacain, Marta, Schober, Sebastian J, Lissat, Andrej, English, William R, Baldini, Nicola, and Heymann, Dominique

Published
2020
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16. Murine Models of Bone Sarcomas

Author

Jacques, Camille, primary, Renema, Nathalie, additional, Ory, Benjamin, additional, Walkley, Carl R., additional, Grigoriadis, Agamemnon E., additional, and Heymann, Dominique, additional

Published
2019
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17. Supplementary Table S1 and S2 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression

Author

Ory, Benjamin, primary, Baud'huin, Marc, primary, Verrecchia, Franck, primary, Royer, Bénédicte Brounais-Le, primary, Quillard, Thibaut, primary, Amiaud, Jérôme, primary, Battaglia, Séverine, primary, Heymann, Dominique, primary, Redini, Francoise, primary, and Lamoureux, Francois, primary

Published
2023
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18. Supplemental Figure 3 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression

Author

Ory, Benjamin, primary, Baud'huin, Marc, primary, Verrecchia, Franck, primary, Royer, Bénédicte Brounais-Le, primary, Quillard, Thibaut, primary, Amiaud, Jérôme, primary, Battaglia, Séverine, primary, Heymann, Dominique, primary, Redini, Francoise, primary, and Lamoureux, Francois, primary

Published
2023
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19. Supplemental Figure 2 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression

Author

Ory, Benjamin, primary, Baud'huin, Marc, primary, Verrecchia, Franck, primary, Royer, Bénédicte Brounais-Le, primary, Quillard, Thibaut, primary, Amiaud, Jérôme, primary, Battaglia, Séverine, primary, Heymann, Dominique, primary, Redini, Francoise, primary, and Lamoureux, Francois, primary

Published
2023
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20. supplemental figure legend from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression

Author

Ory, Benjamin, primary, Baud'huin, Marc, primary, Verrecchia, Franck, primary, Royer, Bénédicte Brounais-Le, primary, Quillard, Thibaut, primary, Amiaud, Jérôme, primary, Battaglia, Séverine, primary, Heymann, Dominique, primary, Redini, Francoise, primary, and Lamoureux, Francois, primary

Published
2023
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21. Supplemental Figure 1 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression

Author

Ory, Benjamin, primary, Baud'huin, Marc, primary, Verrecchia, Franck, primary, Royer, Bénédicte Brounais-Le, primary, Quillard, Thibaut, primary, Amiaud, Jérôme, primary, Battaglia, Séverine, primary, Heymann, Dominique, primary, Redini, Francoise, primary, and Lamoureux, Francois, primary

Published
2023
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22. 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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23. Supplementary Data 1 from Zoledronic Acid Potentiates mTOR Inhibition and Abolishes the Resistance of Osteosarcoma Cells to RAD001 (Everolimus): Pivotal Role of the Prenylation Process

Author

Moriceau, Gatien, primary, Ory, Benjamin, primary, Mitrofan, Laura, primary, Riganti, Chiara, primary, Blanchard, Frédéric, primary, Brion, Régis, primary, Charrier, Céline, primary, Battaglia, Séverine, primary, Pilet, Paul, primary, Denis, Marc G., primary, Shultz, Leonard D., primary, Mönkkönen, Jukka, primary, Rédini, Françoise, primary, and Heymann, Dominique, primary

Published
2023
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24. Data from Zoledronic Acid Potentiates mTOR Inhibition and Abolishes the Resistance of Osteosarcoma Cells to RAD001 (Everolimus): Pivotal Role of the Prenylation Process

Author

Moriceau, Gatien, primary, Ory, Benjamin, primary, Mitrofan, Laura, primary, Riganti, Chiara, primary, Blanchard, Frédéric, primary, Brion, Régis, primary, Charrier, Céline, primary, Battaglia, Séverine, primary, Pilet, Paul, primary, Denis, Marc G., primary, Shultz, Leonard D., primary, Mönkkönen, Jukka, primary, Rédini, Françoise, primary, and Heymann, Dominique, primary

Published
2023
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27. Supplementary Data 2 from Zoledronic Acid Potentiates mTOR Inhibition and Abolishes the Resistance of Osteosarcoma Cells to RAD001 (Everolimus): Pivotal Role of the Prenylation Process

Author

Moriceau, Gatien, primary, Ory, Benjamin, primary, Mitrofan, Laura, primary, Riganti, Chiara, primary, Blanchard, Frédéric, primary, Brion, Régis, primary, Charrier, Céline, primary, Battaglia, Séverine, primary, Pilet, Paul, primary, Denis, Marc G., primary, Shultz, Leonard D., primary, Mönkkönen, Jukka, primary, Rédini, Françoise, primary, and Heymann, Dominique, primary

Published
2023
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28. 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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29. 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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30. Supplementary Data 3 from Zoledronic Acid Potentiates mTOR Inhibition and Abolishes the Resistance of Osteosarcoma Cells to RAD001 (Everolimus): Pivotal Role of the Prenylation Process

Author

Moriceau, Gatien, primary, Ory, Benjamin, primary, Mitrofan, Laura, primary, Riganti, Chiara, primary, Blanchard, Frédéric, primary, Brion, Régis, primary, Charrier, Céline, primary, Battaglia, Séverine, primary, Pilet, Paul, primary, Denis, Marc G., primary, Shultz, Leonard D., primary, Mönkkönen, Jukka, primary, Rédini, Françoise, primary, and Heymann, Dominique, primary

Published
2023
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31. 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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34. Origin and Therapies of Osteosarcoma

Author

Moukengue, Brice, primary, Lallier, Morgane, additional, Marchandet, Louise, additional, Baud’huin, Marc, additional, Verrecchia, Franck, additional, Ory, Benjamin, additional, and Lamoureux, Francois, additional

Published
2022
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35. 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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38. 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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40. Involvement of the TGF-β Signaling Pathway in the Development of YAP-Driven Osteosarcoma Lung Metastasis

Author

Morice, Sarah, Danieau, Geoffroy, Tesfaye, Robel, Mullard, Mathilde, Brion, Régis, Dupuy, Maryne, Ory, Benjamin, Brounais-Le Royer, Bénédicte, Corre, Isabelle, Redini, Françoise, Verrecchia, Franck, 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), Centre hospitalier universitaire de Nantes (CHU Nantes), and CORRE, Isabelle

Subjects
[SDV] Life Sciences [q-bio], Oncology, Hippo, TGF-b/Smad3, TEAD, osteosarcoma, [SDV]Life Sciences [q-bio], lung metastases, YAP, Original Research, TGF-β/Smad3
Abstract

Background The poor survival rate of patients with osteosarcoma (OS), specifically with metastases at diagnosis, undergoes the urgency to develop new therapeutic strategies. Although we recently demonstrated the key role of YAP/TEAD signaling in the growth of OS primary tumor, the molecular mechanisms by which YAP regulates metastases development remain poorly understood. Methods The molecular mechanisms by which YAP regulates metastases development were studied using an overexpression of mutated forms of YAP able or not able to interact with TEAD. Molecular signatures were identified using RNA-sequencing analysis and gene set enrichment. Interactions between YAP and Smad3 were studied using proximity ligation assay (PLA), immunoprecipitation, and promoter/specific gene assays. The involvement of the TGF-β pathway in the ability of YAP to stimulate metastatic development in vivo was studied using an inhibitor of the TGF-β cascade in a preclinical model of OS and in vitro on the ability of OS cells to migrate and invade. Results Our work shows that a high YAP expression is associated with the presence of lung metastases which predicts a poor prognosis. Molecular analysis indicates that TGF-β signaling is involved in YAP-driven osteosarcoma cell pro-migratory phenotype, epithelial mesenchymal transition, cell migration, and in vivo lung metastasis development. Regardless of its ability to bind to TEAD, YAP interacts with Smad3 and stimulates the transcriptional activity of TGF-β/Smad3, thereby enhancing the ability of TGF-β to stimulate lung metastasis development. Conclusions We demonstrated the crucial involvement of the TGF-β/Smad3 signaling pathway in YAP-driven lung metastasis development in OS.

Published
2021

42. List of Contributors

Author

Alix-Panabieres, Catherine, primary, Arlt, Matthias J.E., additional, Bataille, Regis, additional, Bedard, Gillian, additional, Berthold, Dominik R., additional, Bianco, Paolo, additional, Blanchard, Frédéric, additional, Blay, Jean-Yves, additional, Bolton, Damien, additional, Bolzoni, Marina, additional, Born, Walter, additional, Botter, Sander M., additional, Bouvier, Corinne, additional, Brounais-Le Royer, Bénédicte, additional, Brown, Nicola J., additional, Buijs, Jeroen T., additional, Camacho, Daniel F., additional, Campbell, Preston, additional, Chappard, Daniel, additional, Chartier, Stephane, additional, Chou, Hong, additional, Chow, Edward, additional, Chow, Ronald, additional, Christoulas, Dimitrios, additional, Cleton-Jansen, Anne-Marie, additional, Clézardin, Philippe, additional, Clohisy, Denis R., additional, Coleman, Robert, additional, Corradini, Nadège, additional, Croset, Martine, additional, de Pinieux, Gonzague, additional, Derbel, Olfa, additional, Desiderio, Vincenzo, additional, Edwards, James R., additional, Elefteriou, Florent, additional, Fealk, Michelle, additional, Flanagan, Adrienne M., additional, Fournier, Pierrick G.J., additional, Fromigué, Olivia, additional, Fuchs, Bruno, additional, Gao, Dingcheng, additional, Gikas, Panagiotis D., additional, Giuliani, Nicola, additional, Gnant, Michael, additional, Gomez-Brouchet, Anne, additional, Gosheger, Georg, additional, Gouin, François, additional, Guise, Theresa A., additional, Harada, Shuko, additional, Hardes, Jendrik, additional, Hauben, Esther I., additional, He, Wei, additional, Herrera, Fernanda G., additional, Heymann, Marie-Françoise, additional, Hicks, David G., additional, Hogendoorn, Pancras C.W., additional, Holen, Ingunn, additional, Ilaslan, Hakan, additional, Isidor, Bertrand, additional, Jacques, Camille, additional, Juàrez, Patricia, additional, Junankar, Simon, additional, Kabelitz, Dieter, additional, Kalyan, Shirin, additional, Kontny, Udo, additional, Knuutila, Sakari, additional, La Noce, Marcella, additional, Lamora, Audrey, additional, Lamoureux, Francois, additional, Lao, Nicholas, additional, Lawrentschuk, Nathan, additional, Lawson, Michelle A., additional, Lecanda, Fernando, additional, Lee, Jiyun, additional, Lézot, Frédéric, additional, Li, Shibo, additional, Lissat, Andrej, additional, Ludwig, Joseph, additional, Määttä, Jorma A., additional, Mallinson, Paul I., additional, Mantyh, Patrick W., additional, Marie, Pierre J., additional, Mavrogenis, Andreas F., additional, Mikkilineni, Himabindu, additional, Mittal, Vivek, additional, Modrowski, Dominique, additional, Munk, Peter L., additional, Navet, Benjamin, additional, Niini, Tarja, additional, O’Donnell, Patrick W., additional, Odri, Guillaume, additional, Ory, Benjamin, additional, Ouellette, Hugue A., additional, Paino, Francesca, additional, Pantel, K., additional, Papaccio, Federica, additional, Papaccio, Gianpaolo, additional, Park, Paul C., additional, Paterson, Alexander H.G., additional, Patiño-García, Ana, additional, Pienta, Kenneth J., additional, Popovic, Marko, additional, Rajarubendra, Nieroshan, additional, Redini, Françoise, additional, Reeves, Kimberley J., additional, Reisinger, Clemens, additional, Riminucci, Mara, additional, Rodriguez, Lidia, additional, Rogers, Michael J., additional, Ruggieri, Pietro, additional, Sacchetti, Benedetto, additional, Seibel, Markus J., additional, Selvarajah, Shamini, additional, Siegal, Gene P., additional, Sousa, Sofia, additional, Squire, Jeremy A., additional, Sternenberger, Andrea R., additional, Streitbuerger, Arne, additional, Stresing, Verena, additional, Sundaram, Murali, additional, Talbot, Julie, additional, Tang, Ping, additional, Tawadros, Thomas, additional, Terpos, Evangelos, additional, Thomas, Christian, additional, Thompson, Erik W., additional, Thompson, Michelle L., additional, Tirabosco, Roberto, additional, Tirino, Virginia, additional, Tirode, Franck, additional, Trichet, Valèrie, additional, van der Horst, Geertje, additional, van der Pluijm, Gabri, additional, Verrecchia, Franck, additional, Walkley, Carl R., additional, Wei, Shi, additional, and Zielenska, Maria, additional

Published
2015
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44. 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

45. FGFR2 signaling underlies p63 oncogenic function in squamous cell carcinoma

Author

Ramsey, Matthew R., Wilson, Catherine, Ory, Benjamin, Rothenberg, S. Michael, Faquin, William, Mills, Alea A., and Ellisen, Leif W.

Subjects
Squamous cell carcinoma -- Physiological aspects -- Genetic aspects, Fibroblast growth factor receptors -- Physiological aspects -- Health aspects, Cancer -- Genetic aspects, Health care industry
Abstract

Oncogenic transcription factors drive many human cancers, yet identifying and therapeutically targeting the resulting deregulated pathways has proven difficult. Squamous cell carcinoma (SCC) is a common and lethal human cancer, [...]

Published
2013
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46. 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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47. A microRNA-dependent program controls p53-independent survival and chemosensitivity in human and murine squamous cell carcinoma

Author

Ory, Benjamin, Ramsey, Matthew R., Wilson, Catherine, Vadysirisack, Douangsone D., Forster, Nicole, Rocco, James W., Rothenberg, S. Michael, and Ellisen, Leif W.

Subjects
Tumor proteins -- Health aspects -- Research -- Genetic aspects -- Care and treatment -- Drug therapy -- Development and progression, MicroRNA -- Health aspects -- Research -- Genetic aspects, Squamous cell carcinoma -- Research -- Development and progression -- Genetic aspects -- Drug therapy -- Care and treatment, Chemotherapy -- Health aspects -- Research, Apoptosis -- Health aspects -- Research -- Genetic aspects, Cancer -- Chemotherapy, DNA binding proteins -- Health aspects -- Research -- Genetic aspects, Health care industry
Abstract

The p53 tumor suppressor, a central mediator of chemosensitivity in normal cells, is functionally inactivated in many human cancers. Therefore, a central challenge in human cancer therapy is the identification of pathways that control tumor cell survival and chemosensitivity in the absence of functional p53. The p53-related transcription factors p63 and p73 exhibit distinct functions--p73 mediates chemosensitivity while p63 promotes proliferation and cell survival--and are both overexpressed in squamous cell carcinomas (SCCs). However, howp63 and p73 interact functionally and govern the balance between prosurvival and proapoptotic programs in SCC remains elusive. Here, we identify a microRNA-dependent mechanism of p63/p73 crosstalk that regulates p53-independent survival of both human and murine SCC.We first discovered that a subset of p63-regulated microRNAs target p73 for inhibition. One of these, miR-193a-5p, expression of which was repressed by p63, was activated by proapoptotic p73 isoforms in both normal cells and tumor cells in vivo. Chemotherapy caused p63/p73-dependent induction of this microRNA, thereby limiting chemosensitivity due to microRNAmediated feedback inhibition of p73. Importantly, inhibiting miR-193a interrupted this feedback and thereby suppressed tumor cell viability and induced dramatic chemosensitivity both in vitro and in vivo. Thus, we have identified a direct, microRNA-dependent regulatory circuit mediating inducible chemoresistance, whose inhibition may provide a new therapeutic opportunity in p53-deficient tumors., Introduction The p53 family transcription factors, including p53 (TP53), p63 (TP63), and p73 (TP73), play key roles in development, tumorigenesis, and the response to DNA damage. The p53 tumor suppressor [...]

Published
2011
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48. Sarcoma treatment in the era of molecular medicine

Author

Grünewald, Thomas G. P., Alonso, Marta, Avnet, Sofia, Banito, Ana, Burdach, Stefan, Cidre-Aranaz, Florencia, Di Pompo, Gemma, Distel, Martin, Dorado-Garcia, Heathcliff, Garcia-Castro, Javier, Gonzalez-Gonzalez, Laura, Grigoriadis, Agamemnon E., Kasan, Merve, Koelsche, Christian, Krumbholz, Manuela, Lecanda, Fernando, Lemma, Silvia, Longo, Dario L., Madrigal-Esquivel, Claudia, Morales-Molina, Alvaro, Musa, Julian, Ohmura, Shunya, Ory, Benjamin, Pereira-Silva, Miguel, Perut, Francesca, Rodriguez, Rene, Seeling, Carolin, Al Shaaili, Nada, Shaabani, Shabnam, Shiavone, Kristina, Sinha, Snehadri, Tomazou, Eleni M., Trautmann, Marcel, Vela, Maria, Versleijen-Jonkers, Yvonne M. H., Visgauss, Julia, Zalacain, Marta, Schober, Sebastian J., Lissat, Andrej, English, William R., Baldini, Nicola, Heymann, Dominique, Department of Oral and Maxillofacial Diseases, University of Helsinki, and HUS Helsinki and Uusimaa Hospital District

Subjects
EARLY METABOLIC-RESPONSE, Cancer Research, GASTROINTESTINAL STROMAL TUMORS, 3122 Cancers, bone sarcoma, CONDITIONALLY REPLICATIVE ADENOVIRUS, INFILTRATING T-CELLS, PATIENT-DERIVED XENOGRAFTS, targeted therapy, CIRCULATING TUMOR-CELLS, molecular diagnostics, SOFT-TISSUE SARCOMA, soft tissue sarcoma, CANCER STEM-CELLS, ENDOTHELIAL GROWTH-FACTOR, LIMB-SALVAGE TREATMENT, molecular medicine
Abstract

Sarcomas are heterogeneous and clinically challenging soft tissue and bone cancers. Although constituting only 1% of all human malignancies, sarcomas represent the second most common type of solid tumors in children and adolescents and comprise an important group of secondary malignancies. More than 100 histological subtypes have been characterized to date, and many more are being discovered due to molecular profiling. Owing to their mostly aggressive biological behavior, relative rarity, and occurrence at virtually every anatomical site, many sarcoma subtypes are in particular difficult-to-treat categories. Current multimodal treatment concepts combine surgery, polychemotherapy (with/without local hyperthermia), irradiation, immunotherapy, and/or targeted therapeutics. Recent scientific advancements have enabled a more precise molecular characterization of sarcoma subtypes and revealed novel therapeutic targets and prognostic/predictive biomarkers. This review aims at providing a comprehensive overview of the latest advances in the molecular biology of sarcomas and their effects on clinical oncology; it is meant for a broad readership ranging from novices to experts in the field of sarcoma.

Published
2020

49. 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

50. 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

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