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143 results on '"Buendia, Marie Annick"'

1. microRNA 193a-5p Regulates Levels of Nucleolar- and Spindle-Associated Protein 1 to Suppress Hepatocarcinogenesis

Author

Roy, Sanchari, Hooiveld, Guido J., Seehawer, Marco, Caruso, Stefano, Heinzmann, Florian, Schneider, Anne T., Frank, Anna K., Cardenas, David Vargas, Sonntag, Roland, Luedde, Mark, Trautwein, Christian, Stein, Ilan, Pikarsky, Eli, Loosen, Sven, Tacke, Frank, Ringelhan, Marc, Avsaroglu, Seda Kilinc, Goga, Andrei, Buendia, Marie-Annick, Vucur, Mihael, Heikenwalder, Mathias, Zucman-Rossi, Jessica, Zender, Lars, Roderburg, Christoph, and Luedde, Tom

Published
2018
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2. LIM-only protein FHL2 activates NF-κB signaling in the control of liver regeneration and hepatocarcinogenesis.

Author

Dahan, Jennifer, Nouët, Yann, Jouvion, Grégory, Levillayer, Florence, Adib-Conquy, Minou, Cassard-Doulcier, Anne-Marie, Tebbi, Ali, Blanc, Fany, Remy, Lauriane, Cairo, Stefano, Werts, Catherine, Si-Tahar, Mustapha, Tordjmann, Thierry, Buendia, Marie-Annick, Wei, Yu, and Chen, Ju

Subjects
Animals, Cell Line, Cytokines, Diethylnitrosamine, Gene Deletion, Humans, LIM-Homeodomain Proteins, Lipopolysaccharides, Liver, Liver Neoplasms, Liver Regeneration, Macrophages, Mice, Mice, Inbred C57BL, Mice, Knockout, Muscle Proteins, NF-kappa B, Signal Transduction, TNF Receptor-Associated Factor 6, Transcription Factors
Abstract

Four-and-a-half LIM-only protein 2 (FHL2) is an important mediator in many signaling pathways. In this study, we analyzed the functions of FHL2 in nuclear factor κB (NF-κB) signaling in the liver. We show that FHL2 enhanced tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) activity in transcriptional activation of NF-κB targets by stabilizing the protein. TRAF6 is a binding partner of FHL2 and an important component of the Toll-like receptor-NF-κB pathway. Knockdown of FHL2 in 293-hTLR4/MD2-CD14 cells impaired lipopolysaccharide (LPS)-induced NF-κB activity, which regulates expression of inflammatory cytokines. Indeed, FHL2(-/-) macrophages showed significantly reduced production of TNF and interleukin 6 (IL-6) following LPS stimulation. TNF and IL-6 are the key cytokines that prime liver regeneration after hepatic injury. Following partial hepatectomy, FHL2(-/-) mice exhibited diminished induction of TNF and IL-6 and delayed hepatocyte regeneration. In the liver, NF-κB signaling orchestrates inflammatory cross talk between hepatocytes and hepatic immune cells that promote chemical hepatocarcinogenesis. We found that deficiency of FHL2 reduced susceptibility to diethylnitrosamine-induced hepatocarcinogenesis, correlating with the activator function of FHL2 in NF-κB signaling. Our findings demonstrate FHL2 as a positive regulator of NF-κB activity in liver regeneration and carcinogenesis and highlight the importance of FHL2 in both hepatocytes and hepatic immune cells.

Published
2013

4. Abstract PO011: Proteomic profiling of childhood liver cancer: identification of novel diagnostic and prognostic biomarkers

Author

Del Río-Álvarez, Álvaro, primary, Carrillo-Reixach, Juan, additional, Royo, Laura, additional, Domingo-Sàbat, Montse, additional, Azkargorta, Mikel, additional, Kapler, Roland, additional, Cairo, Stefano, additional, Vokuhl, Christian, additional, de Krijger, Ronald, additional, Alaggio, Rita, additional, Garrido, Marta, additional, Guillen, Gabriela, additional, Sábado, Constantino, additional, Guerra, Laura, additional, Hernandez, Francisco, additional, Mateos, Maria Elena, additional, López-Satamaría, Manuel, additional, Torres, Barbara, additional, Abad, Maria Pilar, additional, Viera, Bajčiová, additional, Czauderna, Piotr, additional, Buendia, Marie Annick, additional, Elortza, Felix, additional, Wheatley, Keith, additional, Morland, Bruce, additional, and Armengol, Carolina, additional

Published
2022
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8. TAK1 Suppresses a NEMO-Dependent but NF-κB-Independent Pathway to Liver Cancer

Author

Bettermann, Kira, Vucur, Mihael, Haybaeck, Johannes, Koppe, Christiane, Janssen, Jörn, Heymann, Felix, Weber, Achim, Weiskirchen, Ralf, Liedtke, Christian, Gassler, Nikolaus, Müller, Michael, de Vos, Rita, Wolf, Monika Julia, Boege, Yannick, Seleznik, Gitta Maria, Zeller, Nicolas, Erny, Daniel, Fuchs, Thomas, Zoller, Stefan, Cairo, Stefano, Buendia, Marie-Annick, Prinz, Marco, Akira, Shizuo, Tacke, Frank, Heikenwalder, Mathias, Trautwein, Christian, and Luedde, Tom

Published
2010
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11. Hepatic Stem-like Phenotype and Interplay of Wnt/β-Catenin and Myc Signaling in Aggressive Childhood Liver Cancer

Author

Cairo, Stefano, Armengol, Carolina, De Reyniès, Aurélien, Wei, Yu, Thomas, Emilie, Renard, Claire-Angélique, Goga, Andrei, Balakrishnan, Asha, Semeraro, Michaela, Gresh, Lionel, Pontoglio, Marco, Strick-Marchand, Hélène, Levillayer, Florence, Nouet, Yann, Rickman, David, Gauthier, Frédéric, Branchereau, Sophie, Brugières, Laurence, Laithier, Véronique, Bouvier, Raymonde, Boman, Françoise, Basso, Giuseppe, Michiels, Jean-François, Hofman, Paul, Arbez-Gindre, Francine, Jouan, Hélène, Rousselet-Chapeau, Marie-Christine, Berrebi, Dominique, Marcellin, Luc, Plenat, François, Zachar, Dominique, Joubert, Madeleine, Selves, Janick, Pasquier, Dominique, Bioulac-Sage, Paulette, Grotzer, Michael, Childs, Margaret, Fabre, Monique, and Buendia, Marie-Annick

Published
2008
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20. MicroRNA therapy inhibits hepatoblastoma growth in vivo by targeting β‐catenin and Wnt signaling

Author

Indersie, Emilie, Lesjean, Sarah, Hooks, Katarzyna B., Sagliocco, Francis, Ernault, Tony, Cairo, Stefano, Merched‐Sauvage, Maria, Rullier, Anne, Le Bail, Brigitte, Taque, Sophie, Grotzer, Michael, Branchereau, Sophie, Guettier, Catherine, Fabre, Monique, Brugières, Laurence, Hagedorn, Martin, Buendia, Marie‐Annick, Grosset, Christophe F., Biothérapies des maladies génétiques et cancers, Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Physiopathologie du cancer du foie, Physiopathologie et traitement des maladies du foie, Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital Paul Brousse-Université Paris-Sud - Paris 11 (UP11), CHU Bordeaux [Bordeaux], Laboratoire d'anatomie pathologique, CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin, Department of Oncology, Universität Zürich [Zürich] = University of Zurich (UZH), Département de chirurgie pédiatrique, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Bicêtre, Virus Hépatotropes et Cancers, Université Paris-Sud - Paris 11 (UP11)-IFR89-EA 3541, Département de cancérologie de l'enfant et de l'adolescent [Gustave Roussy], Institut Gustave Roussy (IGR), Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM), XenTech [Evry], Department of Morphology, Surgery and Experimental Medicine [Ferrara Italy] (School of Medicine), Università degli Studi di Ferrara (UniFE), Service de pathologie [Bordeaux], Université Bordeaux Segalen - Bordeaux 2-CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin, Service d'Hématologie et d'Oncologie pédiatrique, CHU Pontchaillou [Rennes], University hospital of Zurich [Zurich], Departement de Pathologie, Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse, Hôpital Bicêtre, Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Bicêtre, Supported by grants from the French National Cancer Institute (grant INCa_TRANSLA_2013_209) to C.F.G, E.I., and M.A.B., French Ministry of Health (grant DGOS/PF4/0013/105) to L.B., Fondation pour la Recherche Medicale (grant DBI20131228566) to C.F.G., Ligue Nationale contre le Cancer to C.F.G., Canceropole Grand Sud-Ouest to C.F.G., the French State in the framework of the ' Investments for the Future' Program IdEx Bordeaux (grant ANR-10-IDEX-03-02) to K.B.H., and the charity associations Eva Pour La Vie, Aidons Marina, Fondation Flavien, and E.S.CA.P.E. to M.H., E.I., and C.F.G., ANR-10-IDEX-0003,IDEX BORDEAUX,Initiative d'excellence de l'Université de Bordeaux(2010), Università degli Studi di Ferrara = University of Ferrara (UniFE), Grosset, Christophe, and Initiative d'excellence de l'Université de Bordeaux - - IDEX BORDEAUX2010 - ANR-10-IDEX-0003 - IDEX - VALID

Subjects
[SDV.CAN] Life Sciences [q-bio]/Cancer, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, Original Article, Original Articles
Abstract

International audience; Hepatoblastoma (HBL) is the most common pediatric liver cancer. In this malignant neoplasm, beta-catenin protein accumulates and increases Wnt signaling due to recurrent activating mutations in the catenin-beta 1 (CTNNB1) gene. Therefore, beta-catenin is a key therapeutic target in HBL. However, controlling beta-catenin production with therapeutic molecules has been challenging. New biological studies could provide alternative therapeutic solutions for the treatment of HBL, especially for advanced tumors and metastatic disease. In this study, we identified microRNAs (miRNAs) that target beta-catenin and block HBL cell proliferation in vitro and tumor growth in vivo. Using our dual-fluorescence-FunREG system, we screened a library of 1,712 miRNA mimics and selected candidates inhibiting CTNNB1 expression through interaction with its untranslated regions. After validating the regulatory effect of nine miRNAs on beta-catenin in HBL cells, we measured their expression in patient samples. Let-7i-3p, miR-449b-3p, miR-624-5p, and miR-885-5p were decreased in tumors compared to normal livers. Moreover, they inhibited HBL cell growth and Wnt signaling activity in vitro partly through beta-catenin down-regulation. Additionally, miR-624-5p induced cell senescence in vitro, blocked experimental HBL growth in vivo, and directly targeted the beta-catenin 3'-untranslated region. Conclusion: Our results shed light on how beta-catenin-regulating miRNAs control HBL progression through Wnt signaling inactivation. In particular, miR-624-5p may constitute a promising candidate for miRNA replacement therapy for HBL patients. (Hepatology Communications 2017;1:168-183).

Published
2017
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24. Somatic mutations of the beta-catenin gene are frequent in mouse and human hepatocellular carcinomas

Author

Coste, Alix de la, Romagnolo, Beatrice, Billuart, Pierre, Renard, Claire-Angelique, Buendia, Marie-Annick, Soubranes, Olivier, Fabre, Monique, Chelly, Jamel, Beldjord, Cherif, Kahn, Axel, and Perret, Christine

Subjects
Gene mutations -- Research, Liver cancer -- Genetic aspects, Science and technology
Abstract

Hepatocellular carcinoma (HCC) is the major primary malignant tumor in the human liver, but the molecular changes leading to liver cell transformation remain largely unknown. The Wnt-[Beta]-catenin pathway is activated in colon cancers and some melanoma cell lines, but has not yet been investigated in HCC. We have examined the status of the [Beta]-catenin gene in different transgenic mouse lines of HCC obtained with the oncogenes c-myc or H-ras. Fifty percent of the hepatic tumors in these transgenic mice had activating somatic mutations within the [Beta]-catenin gene similar to those found in colon cancers and melanomas. These alterations in the [Beta]-catenin gene (point mutations or deletions) lead to a disregulation of the signaling function of [Beta]-catenin and thus to carcinogenesis. We then analyzed human HCCs and found similar mutations in eight of 31 (26%) human liver tumors tested and in HepG2 and HuH6 hepatoma cells. The mutations led to the accumulation of [Beta]-catenin in the nucleus. Thus alterations in the [Beta]-catenin gene frequently are selected for during liver tumorigenesis and suggest that disregulation of the Wnt-[Beta]-catenin pathway is a major event in the development of HCC in humans and mice.

Published
1998

27. Frequent activation of N-myc genes by hepadnavirus insertion in woodchuck live tumours

Author

Fourel, Genevieve, Trepo, Christian, Bougueleret, Lydie, Henglein, Berthold, Ponzetto, Antonio, Tiollais, Pierre, and Buendia, Marie-Annick

Subjects
Hepatitis viruses -- Physiological aspects, Marmots -- Genetic aspects, Liver cancer -- Genetic aspects, Oncogenic viruses -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Published
1990

29. LIM-Only Protein FHL2 Is a Negative Regulator of Transforming Growth Factor β1 Expression

Author

Dahan, Jennifer, primary, Levillayer, Florence, additional, Xia, Tian, additional, Nouët, Yann, additional, Werts, Catherine, additional, Fanton d'Andon, Martine, additional, Adib-Conquy, Minou, additional, Cassard-Doulcier, Anne-Marie, additional, Khanna, Varun, additional, Chen, Ju, additional, Tordjmann, Thierry, additional, Buendia, Marie-Annick, additional, Jouvion, Grégory, additional, and Wei, Yu, additional

Published
2017
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30. Reprogramming of miRNA networks in cancer and leukemia

Author

Volinia, Stefano, Galasso, Marco, Costinean, Stefan, Tagliavini, Luca, Gamberoni, Giacomo, Drusco, Alessandra, Marchesini, Jlenia, Mascellani, Nicoletta, Sana, Maria Elena, Jarour, Ramzey Abu, Desponts, Caroline, Teitell,Michael, Baffa, Raffaele, Aqeilan, Rami, Iorio, Marilena V., Taccioli, Cristian, Garzon, Ramiro, Di Leva, Gianpiero, Fabbri, Muller, Catozzi, Marco, Previati, Maurizio, Ambs, Stefan, Palumbo, Tiziana, Garofalo, Michela, Veronese, Angelo, Bottoni, Arianna, Gasparini, Pierluigi, Harris, Curtis C., Visone, Rosa, Pekarsky, Yuri, Chapelle, Albert de la, Bloomston, Mark, Dillhoff, Mary, Rassenti, Laura Z., Kipps, Thomas J., Huebner, Kay, Pichiorri, Flavia, Lenze, Dido, Cairo, Stefano, Buendia, Marie-Annick, Pineau, Pascal, Dejean, Anne, Zanesi, Nicola, Rossi, Simona, Calin, George A., Chang-Gong Liu, Palatini, Jeff, Negrini, Massimo, Vecchione, Andrea, Rosenberg, Anne, and Croce, Carlo M.

Subjects
MicroRNA -- Research, Cancer -- Genetic aspects, Gene expression -- Analysis, Cancer -- Research, Health
Published
2010

31. Single-Nucleotide Resolution Mapping of Hepatitis B Virus Promoters in Infected Human Livers and Hepatocellular Carcinoma

Author

Altinel, Kübra, primary, Hashimoto, Kosuke, additional, Wei, Yu, additional, Neuveut, Christine, additional, Gupta, Ishita, additional, Suzuki, Ana Maria, additional, Dos Santos, Alexandre, additional, Moreau, Pierrick, additional, Xia, Tian, additional, Kojima, Soichi, additional, Kato, Sachi, additional, Takikawa, Yasuhiro, additional, Hidaka, Isao, additional, Shimizu, Masahito, additional, Matsuura, Tomokazu, additional, Tsubota, Akihito, additional, Ikeda, Hitoshi, additional, Nagoshi, Sumiko, additional, Suzuki, Harukazu, additional, Michel, Marie-Louise, additional, Samuel, Didier, additional, Buendia, Marie Annick, additional, Faivre, Jamila, additional, and Carninci, Piero, additional

Published
2016
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32. CAGE profiling of ncRNAs in hepatocellular carcinoma reveals widespread activation of retroviral LTR promoters in virus-induced tumors

Author

Hashimoto, Kosuke, primary, Suzuki, Ana Maria, additional, Dos Santos, Alexandre, additional, Desterke, Christophe, additional, Collino, Agnese, additional, Ghisletti, Serena, additional, Braun, Emilie, additional, Bonetti, Alessandro, additional, Fort, Alexandre, additional, Qin, Xian-Yang, additional, Radaelli, Enrico, additional, Kaczkowski, Bogumil, additional, Forrest, Alistair R.R., additional, Kojima, Soichi, additional, Samuel, Didier, additional, Natoli, Gioacchino, additional, Buendia, Marie Annick, additional, Faivre, Jamila, additional, and Carninci, Piero, additional

Published
2015
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33. Correction: Corrigendum: Massive gene amplification drives paediatric hepatocellular carcinoma caused by bile salt export pump deficiency

Author

Iannelli, Fabio, primary, Collino, Agnese, additional, Sinha, Shruti, additional, Radaelli, Enrico, additional, Nicoli, Paola, additional, D’Antiga, Lorenzo, additional, Sonzogni, Aurelio, additional, Faivre, Jamila, additional, Buendia, Marie Annick, additional, Sturm, Ekkehard, additional, Thompson, Richard J., additional, Knisely, A. S., additional, Natoli, Gioacchino, additional, Ghisletti, Serena, additional, and Ciccarelli, Francesca D., additional

Published
2015
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34. recherche dans le carcinome hépatocellulaire

Author

Zucman-Rossi, Jessica, Clément, Bruno, Buendia, Marie-Annick, Lerat, Hervé, van Beers, Bernard, Bedossa, Pierre, Taieb, Julien, Rosenbaum, Jean, Zucman-Rossi, Jessica, Génomique Fonctionnelle des Tumeurs Solides (U1162), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Détoxication et réparation tissulaire, Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Oncogenèse et Virologie Moléculaire, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Mondor de recherche biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Service d'imagerie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Beaujon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Gènes et pression artérielle (INSERM U772), Collège de France (CdF (institution))-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'Anatomo-Pathologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Hôpital Beaujon [AP-HP], Service d'hépatogastro-entérologie et d'oncologie digestive, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Fibrose hépatique et cancer du foie, and Université Bordeaux Segalen - Bordeaux 2-IFR66-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
test diagnostiques, MESH: Humans, voie de carcinogenèse, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, MESH: Information Dissemination, digestive system diseases, [SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, MESH: Precancerous Conditions, MESH: Research, MESH: Liver Neoplasms, MESH: Tumor Markers, Biological, recherche, MESH: Liver Cirrhosis, MESH: Carcinoma, Hepatocellular, carcinome hépatocellulaire
Abstract

International audience; Hepatocellular carcinogenesis is usually the result of a muti-step process. It begins with an exposure to various risk factors; followed by the development of a chronic hepatitis and cirrhosis that is a pre-neoplastic step; and finally after the occurrence of an hepatocellular carcinoma (HCC), different molecular events control aggressiveness of the tumors. The aim of this work was to identify in the international context, forces and priorities of the fundamental and translational HCC research.

Published
2009
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35. Abstract 2337: Loss of the LIM-only protein FHL2 enhances TGF-β expression and fibrogenesis

Author

Dahan, Jennifer, primary, Levillayer, Florence, additional, Werts, Catherine, additional, Jouvion, Grégory, additional, Nouët, Yann, additional, Adib-Conquy, Minou, additional, Cassard-Doulcier, Anne-Marie, additional, Xia, Tian, additional, Chen, Ju, additional, Tordjmann, Thierry, additional, Buendia, Marie-Annick, additional, and Wei, Yu, additional

Published
2014
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36. This title is unavailable for guests, please login to see more information.

Author

Dahan, Jennifer, Dahan, Jennifer, Nouët, Yann, Jouvion, Grégory, Levillayer, Florence, Adib-Conquy, Minou, Cassard-Doulcier, Anne-Marie, Tebbi, Ali, Blanc, Fany, Remy, Lauriane, Cairo, Stefano, Werts, Catherine, Si-Tahar, Mustapha, Tordjmann, Thierry, Buendia, Marie-Annick, Wei, Yu, Chen, Ju, Dahan, Jennifer, Dahan, Jennifer, Nouët, Yann, Jouvion, Grégory, Levillayer, Florence, Adib-Conquy, Minou, Cassard-Doulcier, Anne-Marie, Tebbi, Ali, Blanc, Fany, Remy, Lauriane, Cairo, Stefano, Werts, Catherine, Si-Tahar, Mustapha, Tordjmann, Thierry, Buendia, Marie-Annick, Wei, Yu, and Chen, Ju

Published
2013

37. Methyltransferase PRMT1 Is a Binding Partner of HBx and a Negative Regulator of Hepatitis B Virus Transcription

Author

Benhenda, Shirine, primary, Ducroux, Aurélie, additional, Rivière, Lise, additional, Sobhian, Bijan, additional, Ward, Michael D., additional, Dion, Sarah, additional, Hantz, Olivier, additional, Protzer, Ulrike, additional, Michel, Marie-Louise, additional, Benkirane, Monsef, additional, Semmes, Oliver J., additional, Buendia, Marie-Annick, additional, and Neuveut, Christine, additional

Published
2013
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41. Tbx3 Is a Downstream Target of the Wnt/β-Catenin Pathway and a Critical Mediator of β-Catenin Survival Functions in Liver Cancer

Author

Renard, Claire-Angélique, primary, Labalette, Charlotte, additional, Armengol, Carolina, additional, Cougot, Delphine, additional, Wei, Yu, additional, Cairo, Stefano, additional, Pineau, Pascal, additional, Neuveut, Christine, additional, de Reyniès, Aurélien, additional, Dejean, Anne, additional, Perret, Christine, additional, and Buendia, Marie-Annick, additional

Published
2007
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49. LIM-Only Protein FHL2 Activates Nκ-B Signaling in the Control of Liver Regeneration and Hepatocarcinogenesis.

Author

Dahan, Jennifer, Nouët, Yann, Jouvion, Grégory, Levillayer, Florence, Adib-Conquy, Minou, Cassard-Doulcier, Anne-Marie, Tebbi, Ali, Blanc, Fany, Remy, Lauriane, Ju Chen, Cairo, Stefano, Werts, Catherine, Si-Tahar, Mustapha, Tordjmann, Thierry, Buendia, Marie-Annick, and Yu Wei

Subjects
LIVER regeneration, TUMOR necrosis factors, MACROPHAGES, LABORATORY mice, LIVER cells
Abstract

Four-and-a-half LIM-only protein 2 (FHL2) is an important mediator in many signaling pathways. In this study, we analyzed the functions of FHL2 in nuclear factor κB (NF-κB) signaling in the liver. We show that FHL2 enhanced tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) activity in transcriptional activation of NF-κB targets by stabilizing the protein. TRAF6 is a binding partner of FHL2 and an important component of the Toll-like receptor--NF-κB pathway. Knockdown of FHL2 in 293-hTLR4/MD2-CD14 cells impaired lipopolysaccharide (LPS)-induced NF-κB activity, which regulates expression of inflammatory cytokines. Indeed, FHL2-/- macrophages showed significantly reduced production of TNF and interleukin 6 (IL-6) following LPS stimulation. TNF and IL-6 are the key cytokines that prime liver regeneration after hepatic injury. Following partial hepatectomy, FHL2-/- mice exhibited diminished induction of TNF and IL-6 and delayed hepatocyte regeneration. In the liver, NF-B signaling orchestrates inflammatory cross talk between hepatocytes and hepatic immune cells that promote chemical hepatocarcinogenesis. We found that deficiency of FHL2 reduced susceptibility to diethylnitrosamine-induced hepatocarcinogenesis, correlating with the activator function of FHL2 in NF-κB signaling. Our findings demonstrate FHL2 as a positive regulator of NF-κB activity in liver regeneration and carcinogenesis and highlight the importance of FHL2 in both hepatocytes and hepatic immune cells. [ABSTRACT FROM AUTHOR]

Published
2013
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50. Liver Cell Transformation in Chronic HBV Infection.

Author

Benhenda, Shirine, Cougot, Delphine, Neuveut, Christine, and Buendia, Marie Annick

Subjects
LIVER cells, CELL transformation, HEPATITIS B virus, LIVER cancer, ONCOGENES, CARCINOGENESIS, CANCER genes, VIRAL proteins
Abstract

Epidemiological studies have provided overwhelming evidence for a causal role of chronic HBV infection in the development of hepatocellular carcinoma (HCC), but the molecular mechanisms underlying virally-induced tumorigenesis remain largely debated. In the absence of a dominant oncogene encoded by the HBV genome, indirect roles have been proposed, including insertional activation of cellular oncogenes by HBV DNA integration, induction of genetic instability by viral integration or by the regulatory protein HBx, and long term effects of viral proteins in enhancing immune-mediated liver disease. In this chapter, we discuss different models of HBV-mediated liver cell transformation based on animal systems of hepadnavirus infection as well as functional studies in hepatocyte and hepatoma cell lines. These studies might help identifying the cellular effectors connecting HBV infection and liver cell transformation. [ABSTRACT FROM AUTHOR]

Published
2009
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