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9 results on '"Mathilde Cadoux"'

1. Monoacylglycerol lipase reprograms hepatocytes and macrophages to promote liver regeneration

Author

Manon Allaire, Rola Al Sayegh, Morgane Mabire, Adel Hammoutene, Matthieu Siebert, Charles Caër, Mathilde Cadoux, JingHong Wan, Aida Habib, Maude Le Gall, Pierre de la Grange, Hervé Guillou, Catherine Postic, Valérie Paradis, Sophie Lotersztajn, and Hélène Gilgenkrantz

Subjects
Hepatology, Gastroenterology, Internal Medicine, Immunology and Allergy
Published
2023
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2. Monoacylglycerol lipase inhibition specifically in macrophages compromises liver regeneration by inducing interferon type 1 that negatively impacts on hepatocyte proliferation

Author

Manon Allaire, Rola Al-Sayegh, Morgane Mabire, Matthieu Siebert, Mathilde Cadoux, JingHong Wan, Maude Le Gall, Catherine Postic, Hervé Guillou, Pierre de la Grange, Sophie Lotersztajn, Hélène Gilgenkrantz, and LESUR, Hélène

Subjects
[SDV] Life Sciences [q-bio], [SDV.TOX] Life Sciences [q-bio]/Toxicology, Hepatology
Abstract

Meeting AbstractOS084

Published
2022

3. Expression of NKG2D ligands is downregulated by beta-catenin signaling and associates with HCC aggressiveness

Author

Rozenn Riou, Angélique Gougelet, Robin Loesch, Cong Trung Nguyen, Nadia Guerra, Julien Calderaro, Jean-Pierre Couty, Jessica Zucman-Rossi, Sandrine Pham, Chantal Desdouets, Stefano Caruso, Sabine Colnot, Séverine Celton-Morizur, Mathilde Cadoux, Céline Pophillat, Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), and Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université de Paris (UP)

Subjects
Adult, Male, 0301 basic medicine, Carcinoma, Hepatocellular, Adolescent, Carcinogenesis, [SDV]Life Sciences [q-bio], Down-Regulation, Biology, GPI-Linked Proteins, Cohort Studies, Mice, Young Adult, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, medicine, Animals, Humans, beta Catenin, ComputingMilieux_MISCELLANEOUS, Aged, Aged, 80 and over, Hepatology, Histocompatibility Antigens Class I, Liver Neoplasms, Intracellular Signaling Peptides and Proteins, Cancer, TCF4, Middle Aged, HCCS, Prognosis, medicine.disease, NKG2D, 3. Good health, Gene Expression Regulation, Neoplastic, Mice, Inbred C57BL, Immunosurveillance, Disease Models, Animal, 030104 developmental biology, ULBP2, Catenin, Cancer research, Intercellular Signaling Peptides and Proteins, Female, 030211 gastroenterology & hepatology, Signal Transduction
Abstract

Background & Aims The NKG2D system is a potent immunosurveillance mechanism in cancer, wherein the activating NK cell receptor (NKG2D) on immune cells recognises its cognate ligands on tumour cells. Herein, we evaluated the expression of NKG2D ligands in hepatocellular carcinoma (HCC), in both humans and mice, taking the genomic features of HCC tumours into account. Methods The expression of NKG2D ligands (MICA, MICB, ULBP1 and ULBP2) was analysed in large human HCC datasets by Fluidigm TaqMan and RNA-seq methods, and in 2 mouse models (mRNA and protein levels) reproducing the features of both major groups of human tumours. Results We provide compelling evidence that expression of the MICA and MICB ligands in human HCC is associated with tumour aggressiveness and poor patient outcome. We also found that the expression of ULBP1 and ULBP2 was associated with poor patient outcome, and was downregulated in CTNNB1-mutated HCCs displaying low levels of inflammation and associated with a better prognosis. We also found an inverse correlation between ULBP1/2 expression levels and the expression of β-catenin target genes in patients with HCC, suggesting a role for β-catenin signalling in inhibiting expression. We showed in HCC mouse models that β-catenin signalling downregulated the expression of Rae-1 NKG2D ligands, orthologs of ULBPs, through TCF4 binding. Conclusions We demonstrate that the expression of NKG2D ligands is associated with aggressive liver tumorigenesis and that the downregulation of these ligands by β-catenin signalling may account for the less aggressive phenotype of CTNNB1-mutated HCC tumours. Lay summary The NKG2D system is a potent immunosurveillance mechanism in cancer. However, its role in hepatocellular carcinoma development has not been widely investigated. Herein, we should that the expression of NKG2D ligands by tumour cells is associated with a more aggressive tumour subtype.

Published
2021
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4. Lect2 Controls Inflammatory Monocytes to Constrain the Growth and Progression of Hepatocellular Carcinoma

Author

Stefano Caruso, Anne-Marie Crain-Denoyelle, Marie Anson, Antoine L’Hermitte, Jessica Zucman-Rossi, Séverine Celton-Morizur, Sandrine Pham, Mathilde Cadoux, Gabrielle Couchy, Satoshi Yamagoe, Chantal Desdouets, Jean-Pierre Couty, Institut Cochin (IC UM3 (UMR 8104 / U1016)), Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), National Institute of Infectious Diseases [Tokyo], Institut Universitaire d'Hématologie (IUH), Université Paris Diderot - Paris 7 (UPD7), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Desdouets, Chantal

Subjects
0301 basic medicine, Carcinoma, Hepatocellular, Receptors, Peptide, medicine.disease_cause, Monocytes, Receptors, G-Protein-Coupled, Mice, 03 medical and health sciences, 0302 clinical medicine, Tumor Cells, Cultured, medicine, Carcinoma, Animals, Humans, Epithelial–mesenchymal transition, Receptor, Inflammation, Tumor microenvironment, Hepatology, Human liver, business.industry, Liver Neoplasms, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, medicine.disease, [SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, digestive system diseases, 3. Good health, Disease Models, Animal, 030104 developmental biology, Hepatocellular carcinoma, Tumor phenotype, Disease Progression, Cancer research, 030211 gastroenterology & hepatology, business, Carcinogenesis
Abstract

International audience; Leukocyte cell-derived chemotaxin-2 (LECT2) was originally identified as a hepatocyte-secreted chemokine-like factor and a positive target of β-catenin signaling. Here, we dissected out the mechanisms by which LECT2 modulates hepatocellular carcinoma (HCC) development using both HCC mouse models and human HCC samples. We have demonstrated that LECT2 exhibits dual abilities as it has profound repercussions on the tumor phenotype itself and the immune microenvironment. Its absence confers Ctnnb-1-mutated tumor hepatocytes a stronger ability to undergo epithelial to mesenchymal transition and fosters the accumulation of pejorative inflammatory monocytes harboring immunosuppressive properties and strong tumor-promoting potential. Consistent with our HCC mouse model, a low level of LECT2 in human HCC is strongly associated with high tumor grade and the presence of inflammatory infiltrates, emphasizing the clinical value of LECT2 in human liver tumorigenesis. Conclusion: Our findings have demonstrated that LECT2 is a key player in liver tumorigenesis because its absence reshapes the tumor microenvironment and the tumor phenotype, revealing LECT2 as a promising immunotherapeutic option for HCC.

Published
2018
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5. Polyploidy spectrum: a new marker in HCC classification

Author

Jean-Pierre Couty, Valérie Paradis, Géraldine Gentric, Miguel Albuquerque, Romain Donne, Christophe Klein, Chantal Desdouets, Antoine L’Hermitte, Jessica Zucman-Rossi, Julien Calderaro, Thomas Guilbert, Mathilde Cadoux, Gabrielle Couchy, Stefano Caruso, Séverine Celton-Morizur, Myriam Bou-Nader, Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Université Sorbonne Paris Cité (USPC), 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), Hôpital Henri Mondor, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Institut Curie [Paris], Unité de génétique et biologie des cancers (U830), Université Paris Descartes - Paris 5 (UPD5)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de neurosciences comportementales et cognitives (LNCC), Centre National de la Recherche Scientifique (CNRS), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Beaujon, Hôpital Beaujon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), UMR INSERM U955, École nationale vétérinaire d'Alfort (ENVA), Université Paris Descartes - Paris 5 (UPD5)-Institut Curie-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de recherche biomédicale Bichat-Beaujon (CRB3), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Hôpital Beaujon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), and Gestionnaire, Hal Sorbonne Université

Subjects
Male, [SDV]Life Sciences [q-bio], medicine.disease_cause, 0302 clinical medicine, molecular pathology, ComputingMilieux_MISCELLANEOUS, Aged, 80 and over, 0303 health sciences, Molecular pathology, Liver Neoplasms, Gastroenterology, Cell Differentiation, hepatocellular carcinoma, Middle Aged, Cell cycle, Prognosis, Cell Transformation, Neoplastic, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Hepatocyte, histopathology, Female, cell cycle, Ploidy, Adult, [SDV.MHEP.AHA] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], Carcinoma, Hepatocellular, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics, Biology, liver, Polyploidy, Young Adult, 03 medical and health sciences, [SDV.CAN] Life Sciences [q-bio]/Cancer, Polyploid, Parenchyma, Biomarkers, Tumor, medicine, [SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], Humans, Lobules of liver, Aged, Cell Proliferation, 030304 developmental biology, Cell Nucleus, Hepatology, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, [SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, digestive system diseases, [SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics, Case-Control Studies, Hepatocytes, Cancer research, Carcinogenesis
Abstract

ObjectivesPolyploidy is a fascinating characteristic of liver parenchyma. Hepatocyte polyploidy depends on the DNA content of each nucleus (nuclear ploidy) and the number of nuclei per cell (cellular ploidy). Which role can be assigned to polyploidy during human hepatocellular carcinoma (HCC) development is still an open question. Here, we investigated whether a specific ploidy spectrum is associated with clinical and molecular features of HCC.DesignPloidy spectra were determined on surgically resected tissues from patients with HCC as well as healthy control tissues. To define ploidy profiles, a quantitative and qualitative in situ imaging approach was used on paraffin tissue liver sections.ResultsWe first demonstrated that polyploid hepatocytes are the major components of human liver parenchyma, polyploidy being mainly cellular (binuclear hepatocytes). Across liver lobules, polyploid hepatocytes do not exhibit a specific zonation pattern. During liver tumorigenesis, cellular ploidy is drastically reduced; binuclear polyploid hepatocytes are barely present in HCC tumours. Remarkably, nuclear ploidy is specifically amplified in HCC tumours. In fact, nuclear ploidy is amplified in HCCs harbouring a low degree of differentiation and TP53 mutations. Finally, our results demonstrated that highly polyploid tumours are associated with a poor prognosis.ConclusionsOur results underline the importance of quantification of cellular and nuclear ploidy spectra during HCC tumorigenesis.

Published
2019
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7. FRI-335-Lect2, a new hepatokine regulating cholesterol metabolism in liver during non-alcoholic fatty liver disease

Author

Nesrine Mabrouk, Catherine Paul, Mathilde Cadoux, Chantal Desdouets, Philippe Gual, Sandrine Pham, Tran Albert, Catherine Postic, Jean-Pierre Couty, Stéphanie Bonnafous, Valentin Derangere, and Fadila Rayah

Subjects
medicine.medical_specialty, Endocrinology, Hepatology, business.industry, Internal medicine, Fatty liver, medicine, Non alcoholic, Disease, Cholesterol metabolism, business, medicine.disease
Published
2019
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9. p38-alpha MAPK couples inflammatory response and proliferation of hepatocytes during acute liver injury

Author

N. Boussetta, Chantal Desdouets, M. Fortier, Séverine Celton-Morizur, Jean-Pierre Couty, and Mathilde Cadoux

Subjects
0301 basic medicine, Acute liver injury, MAPK/ERK pathway, 03 medical and health sciences, 030104 developmental biology, Hepatology, business.industry, p38 mitogen-activated protein kinases, Inflammatory response, Alpha (ethology), Medicine, Pharmacology, business
Published
2017
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