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1. Treatment of HCC with claudin-1-specific antibodies suppresses carcinogenic signaling and reprograms the tumor microenvironment

Author

Roehlen, Natascha, Muller, Marion, Nehme, Zeina, Crouchet, Emilie, Jühling, Frank, Del Zompo, Fabio, Cherradi, Sara, Duong, Francois H.T., Almeida, Nuno, Saviano, Antonio, Fernández-Vaquero, Mirian, Riedl, Tobias, El Saghire, Houssein, Durand, Sarah C., Ponsolles, Clara, Oudot, Marine A., Martin, Romain, Brignon, Nicolas, Felli, Emanuele, Pessaux, Patrick, Lallement, Antonin, Davidson, Irwin, Bandiera, Simonetta, Thumann, Christine, Marchand, Patrice, Moll, Solange, Nicolay, Brandon, Bardeesy, Nabeel, Hoshida, Yujin, Heikenwälder, Mathias, Iacone, Roberto, Toso, Alberto, Meyer, Markus, Elson, Greg, Schweighoffer, Tamas, Teixeira, Geoffrey, Zeisel, Mirjam B., Laquerriere, Patrice, Lupberger, Joachim, Schuster, Catherine, Mailly, Laurent, and Baumert, Thomas F.

Published
2023
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2. A human liver cell-based system modeling a clinical prognostic liver signature for therapeutic discovery

Author

Crouchet, Emilie, Bandiera, Simonetta, Fujiwara, Naoto, Li, Shen, El Saghire, Hussein, Fernández-Vaquero, Mirian, Riedl, Tobias, Sun, Xiaochen, Hirschfield, Hadassa, Jühling, Frank, Zhu, Shijia, Roehlen, Natascha, Ponsolles, Clara, Heydmann, Laura, Saviano, Antonio, Qian, Tongqi, Venkatesh, Anu, Lupberger, Joachim, Verrier, Eloi R., Sojoodi, Mozhdeh, Oudot, Marine A., Duong, François H. T., Masia, Ricard, Wei, Lan, Thumann, Christine, Durand, Sarah C., González-Motos, Victor, Heide, Danijela, Hetzer, Jenny, Nakagawa, Shigeki, Ono, Atsushi, Song, Won-Min, Higashi, Takaaki, Sanchez, Roberto, Kim, Rosa S., Bian, C. Billie, Kiani, Karun, Croonenborghs, Tom, Subramanian, Aravind, Chung, Raymond T., Straub, Beate K., Schuppan, Detlef, Ankavay, Maliki, Cocquerel, Laurence, Schaeffer, Evelyne, Goossens, Nicolas, Koh, Anna P., Mahajan, Milind, Nair, Venugopalan D., Gunasekaran, Ganesh, Schwartz, Myron E., Bardeesy, Nabeel, Shalek, Alex K., Rozenblatt-Rosen, Orit, Regev, Aviv, Felli, Emanuele, Pessaux, Patrick, Tanabe, Kenneth K., Heikenwälder, Mathias, Schuster, Catherine, Pochet, Nathalie, Zeisel, Mirjam B., Fuchs, Bryan C., Hoshida, Yujin, and Baumert, Thomas F.

Published
2021
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3. Combined Analysis of Metabolomes, Proteomes, and Transcriptomes of Hepatitis C Virus–Infected Cells and Liver to Identify Pathways Associated With Disease Development

Author

Lupberger, Joachim, Croonenborghs, Tom, Roca Suarez, Armando Andres, Van Renne, Nicolaas, Jühling, Frank, Oudot, Marine A., Virzì, Alessia, Bandiera, Simonetta, Jamey, Carole, Meszaros, Gergö, Brumaru, Daniel, Mukherji, Atish, Durand, Sarah C., Heydmann, Laura, Verrier, Eloi R., El Saghire, Hussein, Hamdane, Nourdine, Bartenschlager, Ralf, Fereshetian, Shaunt, Ramberger, Evelyn, Sinha, Rileen, Nabian, Mohsen, Everaert, Celine, Jovanovic, Marko, Mertins, Philipp, Carr, Steven A., Chayama, Kazuaki, Dali-Youcef, Nassim, Ricci, Romeo, Bardeesy, Nabeel M., Fujiwara, Naoto, Gevaert, Olivier, Zeisel, Mirjam B., Hoshida, Yujin, Pochet, Nathalie, and Baumert, Thomas F.

Published
2019
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4. Hepatocellular carcinoma chemoprevention by targeting the angiotensin-converting enzyme and EGFR transactivation

Author

Crouchet, Emilie, primary, Li, Shen, additional, Sojoodi, Mozhdeh, additional, Bandiera, Simonetta, additional, Fujiwara, Naoto, additional, El Saghire, Hussein, additional, Zhu, Shijia, additional, Qian, Tongqi, additional, Rasha, Fahmida Akter, additional, Del Zompo, Fabio, additional, Barrett, Stephen C., additional, Schaeffer, Eugénie, additional, Oudot, Marine A., additional, Ponsolles, Clara, additional, Durand, Sarah C., additional, Ghoshal, Sarani, additional, Arora, Gunisha, additional, Giannone, Fabio, additional, Chung, Raymond T., additional, Slovic, Nevena, additional, Van Renne, Nicolaas, additional, Felli, Emanuele, additional, Pessaux, Patrick, additional, Lupberger, Joachim, additional, Pochet, Nathalie, additional, Schuster, Catherine, additional, Tanabe, Kenneth K., additional, Hoshida, Yujin, additional, Fuchs, Bryan C., additional, and Baumert, Thomas F., additional

Published
2022
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5. Mutation in a primate-conserved retrotransposon reveals a noncoding RNA as a mediator of infantile encephalopathy

Author

Cartault, François, Munier, Patrick, Benko, Edgar, Desguerre, Isabelle, Hanein, Sylvain, Boddaert, Nathalie, Bandiera, Simonetta, Vellayoudom, Jeanine, Krejbich-Trotot, Pascale, Bintner, Marc, Hoarau, Jean-Jacques, Girard, Muriel, Génin, Emmanuelle, de Lonlay, Pascale, Fourmaintraux, Alain, Naville, Magali, Rodriguez, Diana, Feingold, Josué, Renouil, Michel, Munnich, Arnold, Westhof, Eric, Fähling, Michael, Lyonnet, Stanislas, and Henrion-Caude, Alexandra

Published
2012

6. Single cell RNA-seq of patient liver tissues uncover HRH2+/CLEC5a high/macro low macrophages as therapeutic target for the treatment of liver fibrosis and cancer prevention

Author

Crouchet, Emilie, primary, Bandiera, Simonetta, additional, Fujiwara, Naoto, additional, Li, Shen, additional, El Saghire, Hussein, additional, Sun, Xiaochen, additional, Hirschfield, Hadassa, additional, Roehlen, Natascha, additional, Jühling, Frank, additional, Saviano, Antonio, additional, Gonzalez-Motos, Victor, additional, Venkatesh, Anu, additional, Ponsolles, Clara, additional, Lupberger, Joachim, additional, Duong, François H.T., additional, Zhu, Shijia, additional, Sojoodi, Mozhdeh, additional, Masia, Ricard, additional, Wei, Lan, additional, Oudot, Marine, additional, Durand, Sarah, additional, Nakagawa, Shigeki, additional, Ono, Atsushi, additional, Song, Won-Min, additional, Higashi, Takaaki, additional, Kim, Rosa S., additional, Bian, C Billie, additional, Croonenborghs, Tom, additional, Chung, Raymond, additional, Heide, Danijela, additional, Hetzer, Jenny, additional, Straub, Beate, additional, Schuppan, Detlef, additional, Koh, Anna P., additional, Mahajan, Milind, additional, Heikenwalder, Mathias, additional, Felli, Emanuele, additional, Pessaux, Patrick, additional, Tanabe, Kenneth K., additional, Schuster, Catherine, additional, Pochet, Nathalie, additional, Zeisel, Mirjam, additional, Fuchs, Bryan C., additional, Hoshida, Yujin, additional, and Baumert, Thomas, additional

Published
2020
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7. A human liver cell-based system modeling a clinical prognostic liver signature combined with single cell RNA-seq for discovery of novel liver disease therapeutics

Author

Crouchet, Emilie, primary, Bandiera, Simonetta, additional, Fujiwara, Naoto, additional, Li, Shen, additional, El Saghire, Hussein, additional, Sun, Xiaochen, additional, Hirschfield, Hadassa, additional, Roehlen, Natascha, additional, Jühling, Frank, additional, Saviano, Antonio, additional, Gonzalez-Motos, Victor, additional, Venkatesh, Anu, additional, Ponsolles, Clara, additional, Verrier, Eloi, additional, Van Renne, Nicolaas, additional, Lupberger, Joachim, additional, Thumann, Christine, additional, Duong, François H.T., additional, Zhu, Shijia, additional, Sojoodi, Mozhdeh, additional, Masia, Ricard, additional, Wei, Lan, additional, Oudot, Marine, additional, Durand, Sarah, additional, Nakagawa, Shigeki, additional, Ono, Atsushi, additional, Song, Won-Min, additional, Higashi, Takaaki, additional, Sanchez, Roberto, additional, Kim, Rosa S., additional, Bian, C. Billie, additional, Kiani, Karun, additional, Croonenborghs, Tom, additional, Subramanian, Aravind, additional, Chung, Raymond, additional, Heide, Danijela, additional, Hetzer, Jenny, additional, Straub, Beate, additional, Schuppan, Detlef, additional, Ankavay, Maliki, additional, Cocquerel, Laurence, additional, Schaeffer, Evelyne, additional, Goossens, Nicolas, additional, Koh, Anna P., additional, Mahajan, Milind, additional, Nair, Venugopalan D., additional, Gunasekaran, Ganesh, additional, Schwartz, Myron, additional, Bardeesy, Nabeel, additional, Shalek, Alex K., additional, Rozenblatt-Rosen, Orit, additional, Regev, Aviv, additional, Heikenwalder, Mathias, additional, Felli, Emanuele, additional, Pessaux, Patrick, additional, Tanabe, Kenneth K., additional, Schuster, Catherine, additional, Pochet, Nathalie, additional, Zeisel, Mirjam, additional, Fuchs, Bryan C., additional, Hoshida, Yujin, additional, and Baumert, Thomas, additional

Published
2020
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8. HCV-Induced Epigenetic Changes Associated With Liver Cancer Risk Persist After Sustained Virologic Response

Author

Hamdane, Nourdine, Jühling, Frank, Crouchet, Emilie, El Saghire, Houssein, Thumann, Christine, Oudot, Marine A., Bandiera, Simonetta, Saviano, Antonio, Ponsolles, Clara, Roca Suarez, Armando Andres, Li, Shen, Fujiwara, Naoto, Ono, Atsushi, Davidson, Irwin, Bardeesy, Nabeel, Schmidl, Christian, Bock, Christoph, Schuster, Catherine, Lupberger, Joachim, Habersetzer, François, Doffoël, Michel, Piardi, Tullio, Sommacale, Daniele, Imamura, Michio, Uchida, Takuro, Ohdan, Hideki, Aikata, Hiroshi, Chayama, Kazuaki, Boldanova, Tujana, Pessaux, Patrick, Fuchs, Bryan C., Hoshida, Yujin, Zeisel, Mirjam B., Duong, François H.T., Baumert, Thomas F., Institut de Recherche sur les Maladies Virales et Hépatiques (IVH), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Pôle hépato-digestif [Strasbourg], Nouvel Hôpital Civil, Hospices Civils de Strasbourg-Institut Hospitalo-Universitaire de strasbourg, Division of Surgical Oncology [Boston, MA, USA], Harvard Medical School [Boston] (HMS)-Massachusetts General Hospital Cancer Center [Boston, MA, USA], Harold C. Simmons Comprehensive Cancer Center [Dallas, TX, États-Unis], University of Texas Southwestern Medical Center [Dallas], Department of Gastroenterology and Metabolism [Hiroshima, Japan] (Applied Life Sciences), Hiroshima University-Institute of Biomedical & Health Sciences [Hiroshima, Japan], Department of Gastroenterological and Transplant Surgery [Hiroshima, Japan], Hiroshima University-Graduate School of Biomedical and Health Sciences [Hiroshima, Japan], Hiroshima University, Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA), Center for Cancer Research [Boston, MA, USA], Massachusetts General Hospital [Boston], Department of Medicine [Boston, MA, USA], Harvard Medical School [Boston] (HMS), CeMM Research Center for Molecular Medicine [Vienna, Austria], Austrian Academy of Sciences (OeAW), Regensburg Centre for Interventional Immunology [Regensburg, Germany] (RCI), University Medical Center of Regensburg [Regensburg, Germany], Department of Laboratory Medicine [Vienna, Austria], Medizinische Universität Wien = Medical University of Vienna, Max Planck Institute for Informatics [Saarbrücken], Unité de chirurgie générale, digestive et endocrinienne [HU Robert Debré, Reims], Université de Reims Champagne-Ardenne (URCA)-Centre Hospitalier Universitaire de Reims (CHU Reims)-Hôpital universitaire Robert Debré [Reims], Department of Biomedicine [Basel], University Hospital Basel [Basel], Division of Gastroenterology and Hepatology [Basel], Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), This work was supported by the ARC (Paris) and the Institut Hospitalo- Universitaire (Strasbourg, TheraHCC IHUARC IHU201301187 to Thomas F. Baumert), the Foundation of the University of Strasbourg and Roche Institute (HEPKIN to Thomas F. Baumert and Yujin Hoshida), the Agence Nationale de Recherches sur le Sida et les Hépatites Virales (2017/1633 to Thomas F. Baumert), the U.S. Department of Defense (W81XWH-16-1-0363 to Yujin Hoshida and Thomas F. Baumert), the Cancéropôle du Grand-Est (AAP Emergence 2017 to Joachim Lupberger), the National Institutes of Health (DK099558 to Yujin Hoshida), and the Research Program on Hepatitis from the Japan Agency for Medical Research and Development, AMED (17fk0210104h0001 to Kazuaki Chayama). This project has received funding from the European Union’s Horizon 2020 research and innovation program under grant agreement 667273 (HEPCAR to Thomas F. Baumert and Joachim Lupberger). This project has received funding from the European Research Council under the European Union’s Horizon 2020 Research and Innovation Program under grant 671231 (HEPCIR to Thomas F. Baumert and Yujin Hoshida). This work has been published under the framework of the LABEX ANR-10-LABX-0028_HEPSYS, and PLAN CANCER 2014–2019 and benefits from a funding from the state managed by the French National Research Agency as part of the Investments for the Future Program, the French National Cancer Institute, and INSERM., ANR-10-IDEX-0002,UNISTRA,Par-delà les frontières, l'Université de Strasbourg(2010), European Project: 667273,H2020,H2020-PHC-2015-two-stage,HEP-CAR(2016), European Project: 671231,H2020,ERC-2014-ADG,HEPCIR(2016), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), daulny, anne, Initiative d'excellence - Par-delà les frontières, l'Université de Strasbourg - - UNISTRA2010 - ANR-10-IDEX-0002 - IDEX - VALID, Mechanisms underlying hepatocellular carcinoma pathogenesis and impact of co-morbidities. - HEP-CAR - - H20202016-01-01 - 2019-12-31 - 667273 - VALID, and Cell circuits as targets and biomarkers for liver disease and cancer prevention - HEPCIR - - H20202016-01-01 - 2020-12-31 - 671231 - VALID

Subjects
Male, Adult, Epigenomics, Carcinoma, Hepatocellular, Sustained Virologic Response, Biopsy, Aucun, Mice, SCID, Hepacivirus, Sciences du Vivant [q-bio]/Médecine humaine et pathologie, Antiviral Agents, Chemoprevention, Article, Epigenesis, Genetic, Cohort Studies, Mice, Random Allocation, Japan, Animals, Humans, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Liver Neoplasms, virus diseases, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, Biomarker, Hepatitis C, Chronic, [SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, digestive system diseases, Europe, Gene Expression Regulation, Neoplastic, Disease Models, Animal, Case-Control Studies, Female, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Sox9
Abstract

BACKGROUND & AIMS: Chronic hepatitis C virus (HCV) infection is an important risk factor for hepatocellular carcinoma (HCC). Despite effective antiviral therapies, the risk for HCC is decreased but not eliminated after a sustained virologic response (SVR) to direct-acting antiviral (DAA) agents, and the risk is higher in patients with advanced fibrosis. We investigated HCV-induced epigenetic alterations that might affect risk for HCC after DAA treatment in patients and mice with humanized livers. METHODS: We performed genome-wide ChIPmentation-based ChIP-Seq and RNA-seq analyses of liver tissues from 6 patients without HCV infection (controls), 18 patients with chronic HCV infection, 8 patients with chronic HCV infection cured by DAA treatment, 13 patients with chronic HCV infection cured by interferon therapy, 4 patients with chronic hepatitis B virus infection, and 7 patients with nonalcoholic steatohepatitis in Europe and Japan. HCV-induced epigenetic modifications were mapped by comparative analyses with modifications associated with other liver disease etiologies. uPA/SCID mice were engrafted with human hepatocytes to create mice with humanized livers and given injections of HCV-infected serum samples from patients; mice were given DAAs to eradicate the virus. Pathways associated with HCC risk were identified by integrative pathway analyses and validated in analyses of paired HCC tissues from 8 patients with an SVR to DAA treatment of HCV infection. RESULTS: We found chronic HCV infection to induce specific genome-wide changes in H3K27ac, which correlated with changes in expression of mRNAs and proteins. These changes persisted after an SVR to DAAs or interferon-based therapies. Integrative pathway analyses of liver tissues from patients and mice with humanized livers demonstrated that HCV-induced epigenetic alterations were associated with liver cancer risk. Computational analyses associated increased expression of SPHK1 with HCC risk. We validated these findings in an independent cohort of patients with HCV-related cirrhosis (n = 216), a subset of which (n = 21) achieved viral clearance. CONCLUSIONS: In an analysis of liver tissues from patients with and without an SVR to DAA therapy, we identified epigenetic and gene expression alterations associated with risk for HCC. These alterations might be targeted to prevent liver cancer in patients treated for HCV infection., Graphical Abstract

Published
2019

9. miR-135a-5p-mediated downregulation of protein tyrosine phosphatase receptor delta is a candidate driver of HCV-associated hepatocarcinogenesis

Author

Van Renne, Nicolaas, Roca Suarez, Armando Andres, Duong, Francois H T, Gondeau, Claire, Calabrese, Diego, Fontaine, Nelly, Ababsa, Amina, Bandiera, Simonetta, Croonenborghs, Tom, Pochet, Nathalie, De Blasi, Vito, Pessaux, Patrick, Piardi, Tullio, Sommacale, Daniele, Ono, Atsushi, Chayama, Kazuaki, Fujita, Masashi, Nakagawa, Hidewaki, Hoshida, Yujin, Zeisel, Mirjam B, Heim, Markus H, Baumert, Thomas F, Lupberger, Joachim, Institut de Recherche sur les Maladies Virales et Hépatiques (IVH), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), University Hospital Basel [Basel], Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB), Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Harvard-MIT Division of Health Sciences and Technology [Cambridge], Massachusetts Institute of Technology (MIT), L'Institut hospitalo-universitaire de Strasbourg (IHU Strasbourg), Institut National de Recherche en Informatique et en Automatique (Inria)-l'Institut de Recherche contre les Cancers de l'Appareil Digestif (IRCAD)-Les Hôpitaux Universitaires de Strasbourg (HUS)-La Fédération des Crédits Mutuels Centre Est (FCMCE)-L'Association pour la Recherche contre le Cancer (ARC)-La société Karl STORZ, Université de Reims Champagne-Ardenne (URCA), Icahn School of Medicine at Mount Sinai [New York] (MSSM), Hiroshima University, RIKEN Center for Integrative Medical Sciences [Yokohama] (RIKEN IMS), RIKEN - Institute of Physical and Chemical Research [Japon] (RIKEN), Interaction virus-hôte et maladies du foie, Philips, Alexandre, and Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)

Subjects
Adult, Male, STAT3 Transcription Factor, Carcinoma, Hepatocellular, Carcinogenesis, [SDV]Life Sciences [q-bio], Blotting, Western, Aucun, Down-Regulation, Hepacivirus, Sciences du Vivant [q-bio]/Médecine humaine et pathologie, Humans, HEPATOCELLULAR CARCINOMA, RNA, Messenger, ComputingMilieux_MISCELLANEOUS, In Situ Hybridization, Fluorescence, Aged, Aged, 80 and over, Hepatology, Liver Neoplasms, Receptor-Like Protein Tyrosine Phosphatases, Class 2, Middle Aged, Hepatitis C, digestive system diseases, [SDV] Life Sciences [q-bio], MicroRNAs, Liver, SIGNALING, HCV, Hepatocytes, Female, Signal Transduction
Abstract

BACKGROUND AND AIMS: HCV infection is a leading risk factor of hepatocellular carcinoma (HCC). However, even after viral clearance, HCC risk remains elevated. HCV perturbs host cell signalling to maintain infection, and derailed signalling circuitry is a key driver of carcinogenesis. Since protein phosphatases are regulators of signalling events, we aimed to identify phosphatases that respond to HCV infection with relevance for hepatocarcinogenesis. METHODS: We assessed mRNA and microRNA (miRNA) expression profiles in primary human hepatocytes, liver biopsies and resections of patients with HCC, and analysed microarray and RNA-seq data from paired liver biopsies of patients with HCC. We revealed changes in transcriptional networks through gene set enrichment analysis and correlated phosphatase expression levels to patient survival and tumour recurrence. RESULTS: We demonstrate that tumour suppressor protein tyrosine phosphatase receptor delta (PTPRD) is impaired by HCV infection in vivo and in HCC lesions of paired liver biopsies independent from tissue inflammation or fibrosis. In liver tissue adjacent to tumour, high PTPRD levels are associated with a dampened transcriptional activity of STAT3, an increase of patient survival from HCC and reduced tumour recurrence after surgical resection. We identified miR-135a-5p as a mechanistic regulator of hepatic PTPRD expression in patients with HCV. CONCLUSIONS: We previously demonstrated that STAT3 is required for HCV infection. We conclude that HCV promotes a STAT3 transcriptional programme in the liver of patients by suppressing its regulator PTPRD via upregulation of miR-135a-5p. Our results show the existence of a perturbed PTPRD-STAT3 axis potentially driving malignant progression of HCV-associated liver disease.

Published
2018

10. Functional microRNA screen uncovers O-linked N-acetylglucosamine transferase as a host factor modulating hepatitis C virus morphogenesis and infectivity

Author

Herzog, Katharina, primary, Bandiera, Simonetta, additional, Pernot, Sophie, additional, Fauvelle, Catherine, additional, Jühling, Frank, additional, Weiss, Amélie, additional, Bull, Anne, additional, Durand, Sarah C, additional, Chane-Woon-Ming, Béatrice, additional, Pfeffer, Sébastien, additional, Mercey, Marion, additional, Lerat, Hervé, additional, Meunier, Jean-Christophe, additional, Raffelsberger, Wolfgang, additional, Brino, Laurent, additional, Baumert, Thomas F, additional, and Zeisel, Mirjam B, additional

Published
2019
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11. Functional microRNA screen uncovers O-linked N-acetylglucosamine transferase as a host factor modulating hepatitis C virus morphogenesis and infectivity.

Author

Herzog, Katharina, Bandiera, Simonetta, Pernot, Sophie, Fauvelle, Catherine, Jühling, Frank, Weiss, Amélie, Bull, Anne, Durand, Sarah C., Chane-Woon-Ming, Béatrice, Pfeffer, Sébastien, Mercey, Marion, Lerat, Hervé, Meunier, Jean-Christophe, Raffelsberger, Wolfgang, Brino, Laurent, Baumert, Thomas F., and Zeisel, Mirjam B.

Subjects
HEPATITIS C virus, TRANSFERASES, SMALL interfering RNA, MICRORNA, MORPHOGENESIS
Published
2020
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12. miR-135a-5p-mediated downregulation of protein tyrosine phosphatase receptor delta is a candidate driver of HCV-associated hepatocarcinogenesis

Author

Van Renne, Nicolaas, primary, Roca Suarez, Armando Andres, additional, Duong, Francois H T, additional, Gondeau, Claire, additional, Calabrese, Diego, additional, Fontaine, Nelly, additional, Ababsa, Amina, additional, Bandiera, Simonetta, additional, Croonenborghs, Tom, additional, Pochet, Nathalie, additional, De Blasi, Vito, additional, Pessaux, Patrick, additional, Piardi, Tullio, additional, Sommacale, Daniele, additional, Ono, Atsushi, additional, Chayama, Kazuaki, additional, Fujita, Masashi, additional, Nakagawa, Hidewaki, additional, Hoshida, Yujin, additional, Zeisel, Mirjam B, additional, Heim, Markus H, additional, Baumert, Thomas F, additional, and Lupberger, Joachim, additional

Published
2017
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14. Hepatitis C Virus-Induced Upregulation of MicroRNA miR-146a-5p in Hepatocytes Promotes Viral Infection and Deregulates Metabolic Pathways Associated with Liver Disease Pathogenesis

Author

Bandiera, Simonetta, primary, Pernot, Sophie, additional, El Saghire, Hussein, additional, Durand, Sarah C., additional, Thumann, Christine, additional, Crouchet, Emilie, additional, Ye, Tao, additional, Fofana, Isabel, additional, Oudot, Marine A., additional, Barths, Jochen, additional, Schuster, Catherine, additional, Pessaux, Patrick, additional, Heim, Markus H., additional, Baumert, Thomas F., additional, and Zeisel, Mirjam B., additional

Published
2016
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16. Clearance of persistent hepatitis C virus infection in humanized mice using a claudin-1-targeting monoclonal antibody

Author

Mailly, Laurent, primary, Xiao, Fei, additional, Lupberger, Joachim, additional, Wilson, Garrick K, additional, Aubert, Philippe, additional, Duong, François H T, additional, Calabrese, Diego, additional, Leboeuf, Céline, additional, Fofana, Isabel, additional, Thumann, Christine, additional, Bandiera, Simonetta, additional, Lütgehetmann, Marc, additional, Volz, Tassilo, additional, Davis, Christopher, additional, Harris, Helen J, additional, Mee, Christopher J, additional, Girardi, Erika, additional, Chane-Woon-Ming, Béatrice, additional, Ericsson, Maria, additional, Fletcher, Nicola, additional, Bartenschlager, Ralf, additional, Pessaux, Patrick, additional, Vercauteren, Koen, additional, Meuleman, Philip, additional, Villa, Pascal, additional, Kaderali, Lars, additional, Pfeffer, Sébastien, additional, Heim, Markus H, additional, Neunlist, Michel, additional, Zeisel, Mirjam B, additional, Dandri, Maura, additional, McKeating, Jane A, additional, Robinet, Eric, additional, and Baumert, Thomas F, additional

Published
2015
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19. La mitochondrie

Author

Bandiera, Simonetta, primary, Barrey, Eric, additional, Ernoult-Lange, Michèle, additional, Gidrol, Xavier, additional, Henrion-Caude, Alexandra, additional, Huang, Lue, additional, Saint-Auret, Gaelle, additional, and Weil, Dominique, additional

Published
2012
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22. AS032 - A human liver cell-based system modeling a clinical prognostic liver signature combined with single cell RNA-seq for discovery of novel liver disease therapeutics.

Author

Crouchet, Emilie, Bandiera, Simonetta, Fujiwara, Naoto, Li, Shen, El Saghire, Hussein, Sun, Xiaochen, Hirschfield, Hadassa, Roehlen, Natascha, Jühling, Frank, Saviano, Antonio, Gonzalez-Motos, Victor, Venkatesh, Anu, Ponsolles, Clara, Verrier, Eloi, Van Renne, Nicolaas, Lupberger, Joachim, Thumann, Christine, Duong, François H.T., Zhu, Shijia, and Sojoodi, Mozhdeh

Subjects
*RNA sequencing, *LIVER diseases, *LIVER, *THERAPEUTICS
Published
2020
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23. Clearance of persistent hepatitis C virus infection using a claudin-1-targeting monoclonal antibody

Author

Mailly, Laurent, Xiao, Fei, Lupberger, Joachim, Wilson, Garrick K., Aubert, Philippe, Duong, François H. T., Calabrese, Diego, Leboeuf, Céline, Fofana, Isabel, Thumann, Christine, Bandiera, Simonetta, Lütgehetmann, Marc, Volz, Tassilo, Davis, Christopher, Harris, Helen J., Mee, Christopher J., Girardi, Erika, Chane-Woon-Ming, Béatrice, Ericsson, Maria, Fletcher, Nicola, Bartenschlager, Ralf, Pessaux, Patrick, Vercauteren, Koen, Meuleman, Philip, Villa, Pascal, Kaderali, Lars, Pfeffer, Sébastien, Heim, Markus H., Neunlist, Michel, Zeisel, Mirjam B., Dandri, Maura, McKeating, Jane A., Robinet, Eric, and Baumert, Thomas F.

Abstract

Hepatitis C virus (HCV) infection is a leading cause of liver cirrhosis and cancer1. Cell entry of HCV2 and other pathogens3-5 is mediated by tight junction (TJ) proteins, but successful therapeutic targeting of TJ proteins has not been reported yet. Using a human liver-chimeric mouse model6 we show that a monoclonal antibody specific for TJ protein claudin-17 eliminates chronic HCV infection without detectable toxicity. This antibody inhibits HCV entry, cell-cell transmission and virus-induced signaling events. Antibody treatment reduces the number of HCV-infected hepatocytes in vivo, highlighting the need for de novo infection via host entry factors to maintain chronic infection. In summary, we demonstrate that an antibody targeting a virus receptor can cure chronic viral infection and uncover TJ proteins as targets for antiviral therapy.

Published
2015
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24. AS143 - Single cell RNA-seq of patient liver tissues uncover HRH2+/CLEC5a high/macro low macrophages as therapeutic target for the treatment of liver fibrosis and cancer prevention.

Author

Crouchet, Emilie, Bandiera, Simonetta, Fujiwara, Naoto, Li, Shen, El Saghire, Hussein, Sun, Xiaochen, Hirschfield, Hadassa, Roehlen, Natascha, Jühling, Frank, Saviano, Antonio, Gonzalez-Motos, Victor, Venkatesh, Anu, Ponsolles, Clara, Lupberger, Joachim, Duong, François H.T., Zhu, Shijia, Sojoodi, Mozhdeh, Masia, Ricard, Wei, Lan, and Oudot, Marine

Subjects
*LIVER cancer, *RNA sequencing, *CANCER prevention, *LIVER, *TISSUES
Published
2020
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25. HCV-Induced Epigenetic Changes Associated With Liver Cancer Risk Persist After Sustained Virologic Response.

Author

Hamdane N, Jühling F, Crouchet E, El Saghire H, Thumann C, Oudot MA, Bandiera S, Saviano A, Ponsolles C, Roca Suarez AA, Li S, Fujiwara N, Ono A, Davidson I, Bardeesy N, Schmidl C, Bock C, Schuster C, Lupberger J, Habersetzer F, Doffoël M, Piardi T, Sommacale D, Imamura M, Uchida T, Ohdan H, Aikata H, Chayama K, Boldanova T, Pessaux P, Fuchs BC, Hoshida Y, Zeisel MB, Duong FHT, and Baumert TF

Subjects
Adult, Animals, Carcinoma, Hepatocellular genetics, Case-Control Studies, Cohort Studies, Disease Models, Animal, Epigenesis, Genetic, Europe, Female, Gene Expression Regulation, Neoplastic, Hepatitis C, Chronic complications, Hepatitis C, Chronic drug therapy, Humans, Japan, Liver Neoplasms pathology, Male, Mice, Mice, SCID, Random Allocation, Sustained Virologic Response, Antiviral Agents therapeutic use, Carcinoma, Hepatocellular virology, Hepatitis C, Chronic pathology, Liver Neoplasms genetics, Liver Neoplasms virology
Abstract

Background & Aims: Chronic hepatitis C virus (HCV) infection is an important risk factor for hepatocellular carcinoma (HCC). Despite effective antiviral therapies, the risk for HCC is decreased but not eliminated after a sustained virologic response (SVR) to direct-acting antiviral (DAA) agents, and the risk is higher in patients with advanced fibrosis. We investigated HCV-induced epigenetic alterations that might affect risk for HCC after DAA treatment in patients and mice with humanized livers., Methods: We performed genome-wide ChIPmentation-based ChIP-Seq and RNA-seq analyses of liver tissues from 6 patients without HCV infection (controls), 18 patients with chronic HCV infection, 8 patients with chronic HCV infection cured by DAA treatment, 13 patients with chronic HCV infection cured by interferon therapy, 4 patients with chronic hepatitis B virus infection, and 7 patients with nonalcoholic steatohepatitis in Europe and Japan. HCV-induced epigenetic modifications were mapped by comparative analyses with modifications associated with other liver disease etiologies. uPA/SCID mice were engrafted with human hepatocytes to create mice with humanized livers and given injections of HCV-infected serum samples from patients; mice were given DAAs to eradicate the virus. Pathways associated with HCC risk were identified by integrative pathway analyses and validated in analyses of paired HCC tissues from 8 patients with an SVR to DAA treatment of HCV infection., Results: We found chronic HCV infection to induce specific genome-wide changes in H3K27ac, which correlated with changes in expression of mRNAs and proteins. These changes persisted after an SVR to DAAs or interferon-based therapies. Integrative pathway analyses of liver tissues from patients and mice with humanized livers demonstrated that HCV-induced epigenetic alterations were associated with liver cancer risk. Computational analyses associated increased expression of SPHK1 with HCC risk. We validated these findings in an independent cohort of patients with HCV-related cirrhosis (n = 216), a subset of which (n = 21) achieved viral clearance., Conclusions: In an analysis of liver tissues from patients with and without an SVR to DAA therapy, we identified epigenetic and gene expression alterations associated with risk for HCC. These alterations might be targeted to prevent liver cancer in patients treated for HCV infection., (Copyright © 2019 AGA Institute. Published by Elsevier Inc. All rights reserved.)

Published
2019
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26. miR-135a-5p-mediated downregulation of protein tyrosine phosphatase receptor delta is a candidate driver of HCV-associated hepatocarcinogenesis.

Author

Van Renne N, Roca Suarez AA, Duong FHT, Gondeau C, Calabrese D, Fontaine N, Ababsa A, Bandiera S, Croonenborghs T, Pochet N, De Blasi V, Pessaux P, Piardi T, Sommacale D, Ono A, Chayama K, Fujita M, Nakagawa H, Hoshida Y, Zeisel MB, Heim MH, Baumert TF, and Lupberger J

Subjects
Adult, Aged, Aged, 80 and over, Blotting, Western, Carcinogenesis metabolism, Carcinoma, Hepatocellular virology, Down-Regulation, Female, Hepatocytes metabolism, Humans, In Situ Hybridization, Fluorescence, Liver pathology, Liver Neoplasms virology, Male, Middle Aged, RNA, Messenger metabolism, STAT3 Transcription Factor metabolism, Signal Transduction, Carcinoma, Hepatocellular metabolism, Hepacivirus pathogenicity, Hepatitis C complications, Liver Neoplasms metabolism, MicroRNAs metabolism, Receptor-Like Protein Tyrosine Phosphatases, Class 2 metabolism
Abstract

Background and Aims: HCV infection is a leading risk factor of hepatocellular carcinoma (HCC). However, even after viral clearance, HCC risk remains elevated. HCV perturbs host cell signalling to maintain infection, and derailed signalling circuitry is a key driver of carcinogenesis. Since protein phosphatases are regulators of signalling events, we aimed to identify phosphatases that respond to HCV infection with relevance for hepatocarcinogenesis., Methods: We assessed mRNA and microRNA (miRNA) expression profiles in primary human hepatocytes, liver biopsies and resections of patients with HCC, and analysed microarray and RNA-seq data from paired liver biopsies of patients with HCC. We revealed changes in transcriptional networks through gene set enrichment analysis and correlated phosphatase expression levels to patient survival and tumour recurrence., Results: We demonstrate that tumour suppressor protein tyrosine phosphatase receptor delta (PTPRD) is impaired by HCV infection in vivo and in HCC lesions of paired liver biopsies independent from tissue inflammation or fibrosis. In liver tissue adjacent to tumour, high PTPRD levels are associated with a dampened transcriptional activity of STAT3, an increase of patient survival from HCC and reduced tumour recurrence after surgical resection. We identified miR-135a-5p as a mechanistic regulator of hepatic PTPRD expression in patients with HCV., Conclusions: We previously demonstrated that STAT3 is required for HCV infection. We conclude that HCV promotes a STAT3 transcriptional programme in the liver of patients by suppressing its regulator PTPRD via upregulation of miR-135a-5p. Our results show the existence of a perturbed PTPRD-STAT3 axis potentially driving malignant progression of HCV-associated liver disease., Competing Interests: Competing interests: None declared., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.)

Published
2018
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27. [Mitochondria, microRNA and RNA interference].

Author

Bandiera S, Barrey E, Ernoult-Lange M, Gidrol X, Henrion-Caude A, Huang L, Saint-Auret G, and Weil D

Subjects
Animals, Argonaute Proteins physiology, Carboxypeptidases physiology, Cells, Cultured, Cytoplasmic Granules physiology, Gene Expression Regulation, Genome, Mitochondrial, Humans, In Situ Hybridization, Mitochondria ultrastructure, Mitochondria, Muscle physiology, Mitochondria, Muscle ultrastructure, Mitochondrial Membranes metabolism, Permeability, Rats, Retinal Pigment Epithelium cytology, MicroRNAs physiology, Mitochondria physiology, RNA Interference physiology
Published
2012
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