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39 results on '"Jalaguier, Stéphan"'

3. RIP140 regulates transcription factor HES1 oscillatory expression and mitogenic activity in colon cancer cells.

Author

Sfeir, Nour, Kajdan, Marilyn, Jalaguier, Stéphan, Bonnet, Sandrine, Teyssier, Catherine, Pyrdziak, Samuel, Yuan, Rong, Bousquet, Emilie, Maraver, Antonio, Bernex, Florence, Pirot, Nelly, Boissière‐Michot, Florence, Castet‐Nicolas, Audrey, Lapierre, Marion, and Cavaillès, Vincent

Abstract

The transcription factor receptor‐interacting protein 140 (RIP140) regulates intestinal homeostasis and tumorigenesis through Wnt signaling. In this study, we investigated its effect on the Notch/HES1 signaling pathway. In colorectal cancer (CRC) cell lines, RIP140 positively regulated HES1 gene expression at the transcriptional level via a recombining binding protein suppressor of hairless (RBPJ)/neurogenic locus notch homolog protein 1 (NICD)‐mediated mechanism. In support of these in vitro data, RIP140 and HES1 expression significantly correlated in mouse intestine and in a cohort of CRC samples, thus supporting the positive regulation of HES1 gene expression by RIP140. Interestingly, when the Notch pathway is fully activated, RIP140 exerted a strong inhibition of HES1 gene transcription controlled by the level of HES1 itself. Moreover, RIP140 directly interacts with HES1 and reversed its mitogenic activity in human CRC cells. In line with this observation, HES1 levels were associated with a better patient survival only when tumors expressed high levels of RIP140. Our data identify RIP140 as a key regulator of the Notch/HES1 signaling pathway, with a dual effect on HES1 gene expression at the transcriptional level and a strong impact on colon cancer cell proliferation. [ABSTRACT FROM AUTHOR]

Published
2024
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9. A Truncated NRIP1 Mutant Amplifies Microsatellite Instability of Colorectal Cancer by Regulating MSH2/MSH6 Expression, and Is a Prognostic Marker of Stage III Tumors

Author

Palassin, Pascale, Lapierre, Marion, Pyrdziak, Samuel, Wagner, Antoine, Stehle, Régine, Corsini, Carole, Duffour, Jacqueline, Bonnet, Sandrine, Boulahtouf, Abdelhay, Rodriguez, Carmen, Ho-Puncheun, Alexandre, Lopez-Crapez, Evelyne, Boissière-Michot, Florence, Bibeau, Frédéric, Thezenas, Simon, Elarouci, Nabila, Selves, Janick, Hoffmann, Jean-Sébastien, Roepman, Paul, Mazard, Thibault, Buhard, Olivier, Duval, Alex, Jalaguier, Stéphan, Cavaillès, Vincent, Castet-Nicolas, Audrey, Institut de Recherche en Cancérologie de Montpellier (IRCM - U1194 Inserm - UM), CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Institut du Cancer de Montpellier (ICM), Ligue Nationale Contre le Cancer - Paris, Ligue Nationnale Contre le Cancer, Institut Universitaire du Cancer de Toulouse - Oncopole (IUCT Oncopole - UMR 1037), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM), Agendia NV, Agendia NV, Amsterdam, Pathologies biliaires, fibrose et cancer du foie [CHU Saint-Antoine], Centre de Recherche Saint-Antoine (CR Saint-Antoine), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Unité de Formation et de Recherche des Sciences Pharmaceutiques et Biologiques, Ligue Nationale Contre le Cancer (LNCC), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM), Pathologies biliaires, fibrose et cancer du foie [CRSA], Centre de Recherche Saint-Antoine (CRSA), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), and Gibier, François

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, [SDV]Life Sciences [q-bio], nutritional and metabolic diseases, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, colorectal cancer, Article, digestive system diseases, [SDV] Life Sciences [q-bio], patient prognosis, mismatch repair, microsatellite instability, neoplasms, RIP140/NRIP1, RC254-282
Abstract

Simple Summary The alteration of mismatch repair (MMR) genes leads to microsatellite instability and plays a key role in colorectal cancer (CRC) pathogenesis and prognosis. The transcription factor NRIP1 is involved in intestinal tumorigenesis and is a good prognostic marker in CRC. In this study, we demonstrate that NRIP1 induces MSH2 and MSH6 MMR gene transcription and reduces microsatellite instability. A dominant-negative truncated NRIP1 mutant amplifies the MMR-deficient phenotype and appears as a key player in MSI-driven tumorigenesis since it significantly correlates with a short overall survival of patients with advanced CRC, especially MLH1-deficient ones. Abstract Microsatellite instability (MSI) is related to the alteration of mismatch repair (MMR) genes and plays a key role in colorectal cancer (CRC) pathogenesis. We previously reported that the transcription factor Nuclear Receptor Interacting Protein 1 (NRIP1) is involved in sporadic intestinal tumorigenesis. The aim of this study was to decipher its role in MSI CRC. By using different mouse models and engineered cell lines, we demonstrated that NRIP1 increased MSH2 and MSH6 MMR gene transcription and mRNA/protein levels. In human CRC cells, NRIP1 expression was associated with decreased MSI and the hypermutator phenotype, and with resistance to chemotherapy drugs. Using a cohort of 194 CRC patients, we detected in 22% of the cases a MSI-induced frameshift mutation in the NRIP1 coding sequence. This genetic alteration generates a truncated protein with a dominant negative activity that increased human CRC cell proliferation and impaired the regulation of MSH2 and MSH6 gene expression. Moreover, the NRIP1 mutant correlated with a decreased overall survival of patients with advanced CRC, especially when MLH1-deficient. By decreasing the expression of MSH2 and MSH6 gene expression, the NRIP1 variant may amplify MLH1-dependent CRC progression and behave as a new prognostic marker of advanced MSI CRC.

Published
2021
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14. RIP140 inhibits glycolysis-dependent proliferation of breast cancer cells by regulating GLUT3 expression through transcriptional crosstalk between hypoxia induced factor and p53

Author

Jacquier, Valentin, primary, Gitenay, Delphine, additional, Fritsch, Samuel, additional, Bonnet, Sandrine, additional, Győrffy, Balázs, additional, Jalaguier, Stéphan, additional, Linares, Laetitia K., additional, Cavaillès, Vincent, additional, and Teyssier, Catherine, additional

Published
2020
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19. The Prognostic Impact of the Aryl Hydrocarbon Receptor (AhR) in Primary Breast Cancer Depends on the Lymph Node Status

Author

Jeschke, Udo, primary, Zhang, Xi, additional, Kuhn, Christina, additional, Jalaguier, Stéphan, additional, Colinge, Jacques, additional, Pfender, Kristina, additional, Mayr, Doris, additional, Ditsch, Nina, additional, Harbeck, Nadia, additional, Mahner, Sven, additional, Sixou, Sophie, additional, and Cavaillès, Vincent, additional

Published
2019
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21. Expression and role of RIP140/NRIP1 in chronic lymphocytic leukemia

Author

Lapierre, Marion, Castet-Nicolas, Audrey, Gitenay, Delphine, Jalaguier, Stéphan, Teyssier, Catherine, Bret, Caroline, Cartron, Guillaume, Moreaux, Jérôme, Cavaillès, Vincent, Institut de Recherche en Cancérologie de Montpellier (IRCM - U1194 Inserm - UM), CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Université de Montpellier (UM), Institut de génétique humaine (IGH), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Dynamique des interactions membranaires normales et pathologiques (DIMNP), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université Montpellier 1 (UM1), Département d'Hématologie Biologique, CHU Montpellier, Montpellier, Larose, Catherine, and Université Montpellier 1 (UM1)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Cancer Research, Cell signaling, [SDV.GEN]Life Sciences [q-bio]/Genetics, Nuclear Proteins, Review, Hematology, [SDV.GEN] Life Sciences [q-bio]/Genetics, Prognosis marker, Leukemia, Lymphocytic, Chronic, B-Cell, Nuclear Receptor Interacting Protein 1, Oncology, Animals, Humans, Chronic lymphocytic leukemia, Molecular Biology, ComputingMilieux_MISCELLANEOUS, RIP140/NRIP1, Adaptor Proteins, Signal Transducing
Abstract

RIP140 is a transcriptional coregulator, (also known as NRIP1), which finely tunes the activity of various transcription factors and plays very important physiological roles. Noticeably, the RIP140 gene has been implicated in the control of energy expenditure, behavior, cognition, mammary gland development and intestinal homeostasis. RIP140 is also involved in the regulation of various oncogenic signaling pathways and participates in the development and progression of solid tumors. During the past years, several papers have reported evidences linking RIP140 to hematologic malignancies. Among them, two recent studies with correlative data suggested that gene expression signatures including RIP140 can predict survival in chronic lymphocytic leukemia (CLL). This review aims to summarize the literature dealing with the expression of RIP140 in CLL and to explore the potential impact of this factor on transcription pathways which play key roles in this pathology.

Published
2015
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22. Histone deacetylase 9 regulates breast cancer cell proliferation and the response to histone deacetylase inhibitors

Author

Lapierre, Marion, primary, Linares, Aurélien, additional, Dalvai, Mathieu, additional, Duraffourd, Céline, additional, Bonnet, Sandrine, additional, Boulahtouf, Abdelhay, additional, Rodriguez, Carmen, additional, Jalaguier, Stéphan, additional, Assou, Said, additional, Orsetti, Beatrice, additional, Balaguer, Patrick, additional, Maudelonde, Thierry, additional, Blache, Philippe, additional, Bystricky, Kerstin, additional, Boulle, Nathalie, additional, and Cavaillès, Vincent, additional

Published
2016
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24. L’effet Warburg

Author

Razungles, Julie, primary, Cavaillès, Vincent, additional, Jalaguier, Stéphan, additional, and Teyssier, Catherine, additional

Published
2013
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38. [The Warburg effect: from theory to therapeutic applications in cancer].

Author

Razungles J, Cavaillès V, Jalaguier S, and Teyssier C

Subjects
Animals, Carcinogenesis metabolism, Carcinogenesis pathology, Cell Proliferation, Cells metabolism, Energy Metabolism, Germany, Glucose metabolism, Glycolysis genetics, History, 19th Century, History, 20th Century, Humans, Mutation, Neoplasms etiology, Neoplasms therapy, Signal Transduction, Models, Theoretical, Neoplasms history
Abstract

Cancer cell metabolism described by Otto Warburg in the thirties became a cancer specific hallmark, also called "Warburg effect". Cancer cells use essentially glucose as fuel, through glycolysis, in order to meet their energy and biomass needs to insure their cell proliferation. Recent advances describe Warburg effect regulation by oncogenes and tumor suppressor genes. Moreover, mutations in some glycolysis enzymes are found in various cancers, highlighting the role of cell metabolism in cancer. In this review, we describe the mechanisms responsible for the Warburg effect at the molecular and cellular level, the role of cell signalling along with the implication of different transcription factors. As a cause or a consequence of tumorigenesis, the Warburg effect is now considered as a promising therapeutic target in the fight against cancer., (© 2013 médecine/sciences – Inserm.)

Published
2013
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39. [RIP140 and hormone signaling].

Author

Castet A, Carascossa S, Duong V, Augereau P, Jalaguier S, and Cavaillès V

Subjects
Adaptor Proteins, Signal Transducing, Animals, Female, Humans, Male, Nuclear Proteins genetics, Nuclear Receptor Interacting Protein 1, Receptors, Estrogen genetics, Transcription, Genetic, Hormones physiology, Nuclear Proteins physiology, Receptors, Estrogen physiology
Abstract

Nuclear hormone receptors belong to a superfamily of ligand-activated transcription factors which regulate fundamental physiological processes. Their activity is controlled by a large number of coregulatory proteins which are, in most cases, recruited by nuclear receptors in the presence of ligand. RIP140 (receptor interacting protein of 140 kDa) was one of the first transcription cofactors to be identified almost ten years ago. This molecule is an atypical cofactor which interacts with agonist-liganded nuclear receptors but negatively regulates their transactivation potential. RIP140 exhibits nine leucine-rich motifs (LxxLL) which mediate the specific docking on the nuclear receptor ligand-binding domain. Transcription repression exerted by this cofactor implicates different mechanisms. Not only it involves a competition with coactivators such as those belonging to the p160 family, but also relies on active intrinsic repression through at least four different domains which allow recruitement of downstream repressors such as histone deacetylases (HDACs) or C-terminal binding proteins (CtBPs). The biological role of RIP140 has been investigated by disrupting the gene in mice. The lack of RIP140 expression in ovaries prevents follicle rupture and ovulation, rising to female infertility. In addition, this cofactor is also required for the control of fat storage and utilization through the regulation of genes involved in thermogenesis. Finally, RIP140 could play a role in the hormonal control of cancer cell proliferation by negatively regulating the activity of estrogen and retinoic acid receptors which are key actors in cancer growth. Interestingly, both estrogens and retinoic acid regulate RIP140 gene expression, revealing an increased level of complexity. In conclusion, RIP140 is an atypical transcription inhibitor which, by repressing nuclear hormone receptor activity, plays fundamental physiopathological roles.

Published
2005
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