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2. ProNGF promotes brain metastasis through TrkA/EphA2 induced Src activation in triple negative breast cancer cells

Author

Cicero, Julien, Trouvilliez, Sarah, Palma, Martine, Ternier, Gaetan, Decoster, Laurine, Happernegg, Eloise, Barois, Nicolas, Van Outryve, Alexandre, Dehouck, Lucie, Bourette, Roland P., Adriaenssens, Eric, Lagadec, Chann, Tarhan, Cagatay Mehmet, Collard, Dominique, Souguir, Zied, Vandenhaute, Elodie, Maubon, Grégory, Sipieter, François, Borghi, Nicolas, Shimizu, Fumitaka, Kanda, Takashi, Giacobini, Paolo, Gosselet, Fabien, Maubon, Nathalie, Le Bourhis, Xuefen, Van Seuningen, Isabelle, Mysiorek, Caroline, and Toillon, Robert-Alain

Published
2023
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6. Chemotherapy-induced ileal crypt apoptosis and the ileal microbiome shape immunosurveillance and prognosis of proximal colon cancer

Author

Roberti, Maria Paula, Yonekura, Satoru, Duong, Connie P. M., Picard, Marion, Ferrere, Gladys, Tidjani Alou, Maryam, Rauber, Conrad, Iebba, Valerio, Lehmann, Christian H. K., Amon, Lukas, Dudziak, Diana, Derosa, Lisa, Routy, Bertrand, Flament, Caroline, Richard, Corentin, Daillère, Romain, Fluckiger, Aurélie, Van Seuningen, Isabelle, Chamaillard, Mathias, Vincent, Audrey, Kourula, Stephanie, Opolon, Paule, Ly, Pierre, Pizzato, Eugénie, Becharef, Sonia, Paillet, Juliette, Klein, Christophe, Marliot, Florence, Pietrantonio, Filippo, Benoist, Stéphane, Scoazec, Jean-Yves, Dartigues, Peggy, Hollebecque, Antoine, Malka, David, Pagès, Franck, Galon, Jérôme, Gomperts Boneca, Ivo, Lepage, Patricia, Ryffel, Bernard, Raoult, Didier, Eggermont, Alexander, Vanden Berghe, Tom, Ghiringhelli, François, Vandenabeele, Peter, Kroemer, Guido, and Zitvogel, Laurence

Published
2020
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10. Galectin-3 modulates epithelial cell adaptation to stress at the ER-mitochondria interface

Author

Coppin, Lucie, Jannin, Arnaud, Ait Yahya, Emilie, Thuillier, Caroline, Villenet, Céline, Tardivel, Meryem, Bongiovanni, Antonino, Gaston, Cécile, de Beco, Simon, Barois, Nicolas, van Seuningen, Isabelle, Durand, Emmanuelle, Bonnefond, Amélie, Vienne, Jean-Claude, Vamecq, Joseph, Figeac, Martin, Vincent, Audrey, Delacour, Delphine, Porchet, Nicole, and Pigny, Pascal

Published
2020
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13. MUC1 Drives the Progression and Chemoresistance of Clear Cell Renal Carcinomas.

Author

Bourdon, Emma, Swierczewski, Thomas, Goujon, Marine, Boukrout, Nihad, Fellah, Sandy, Van der Hauwaert, Cynthia, Larrue, Romain, Lefebvre, Bruno, Van Seuningen, Isabelle, Cauffiez, Christelle, Pottier, Nicolas, and Perrais, Michaël

Subjects
DISEASE progression, RENAL cell carcinoma, CANCER invasiveness, ANTINEOPLASTIC agents, CELL physiology, RISK assessment, CELL motility, MOLECULAR biology, TREATMENT effectiveness, GLYCOPROTEINS, CELL proliferation, RESEARCH funding, DRUG resistance in cancer cells, PHARMACODYNAMICS
Abstract

Simple Summary: Clear cell renal cell carcinoma (ccRCC) is the main histotype of kidney cancer, which is typically highly resistant to conventional systemic therapies and also to targeted therapies. Identifying the actors and deciphering the molecular mechanisms that lead to tumor progression and/or chemoresistance is an important step in developing new therapeutic strategies to cure ccRCC. In this context, we focused our attention on MUC1, a membrane-bound mucin, which is overexpressed in two-thirds of cancers and known to play a role in tumor progression, chemoresistance, and the establishment of an immunosuppressive microenvironment. In this study, we show that MUC1 overexpression increases the proliferation, invasion, and migration of ccRCC cells and is involved in mediating resistance to conventional and targeted therapies. Overall, our data suggest that MUC1 silencing may represent a potential therapeutic option for ccRCC. While the transmembrane glycoprotein mucin 1 (MUC1) is clustered at the apical borders of normal epithelial cells, with transformation and loss of polarity, MUC1 is found at high levels in the cytosol and is uniformly distributed over the entire surface of carcinoma cells, where it can promote tumor progression and adversely affects the response to therapy. Clear cell renal cell carcinoma (ccRCC), the main histotype of kidney cancer, is typically highly resistant to conventional and targeted therapies for reasons that remain largely unknown. In this context, we investigated whether MUC1 also plays a pivotal role in the cellular and molecular events driving ccRCC progression and chemoresistance. We showed, using loss- and gain-of-function approaches in ccRCC-derived cell lines, that MUC1 not only influences tumor progression but also induces a multi-drug-resistant profile reminiscent of the activation of ABC drug efflux transporters. Overall, our results suggest that targeting MUC1 may represent a novel therapeutic approach to limit ccRCC progression and improve drug sensitivity. [ABSTRACT FROM AUTHOR]

Published
2024
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14. A novel anti-galectin-9 immunotherapy limits the early progression of pancreatic neoplastic lesions in transgenic mice.

Author

Quilbe, Alexandre, Mustapha, Rami, Duchêne, Belinda, Kumar, Abhishek, Werkmeister, Elisabeth, Leteurtre, Emmanuelle, Moralès, Olivier, Jonckheere, Nicolas, Van Seuningen, Isabelle, and Delhem, Nadira

Subjects
PANCREATIC intraepithelial neoplasia, PANCREATIC tumors, TRANSGENIC mice, REGULATORY T cells, IMMUNE checkpoint inhibitors, PRECANCEROUS conditions, T cells
Abstract

Background: Pancreatic adenocarcinoma (PDAC) is a devastating disease with an urgent need for therapeutic innovation. Immune checkpoint inhibition has shown promise in a variety of solid tumors, but most clinical trials have failed to demonstrate clinical efficacy in PDAC. This low efficacy is partly explained by a highly immunosuppressive microenvironment, which dampens anti-tumor immunity through the recruitment or induction of immunosuppressive cells, particularly regulatory T cells (Tregs). In this context, our laboratory has developed a novel immunotherapeutic strategy aimed at inhibiting the suppressive activity of Tregs, based on a patented (EP3152234B1) monoclonal antibody (mAb) targeting galectin-9 (LGALS9). Materials and methods: CD4+ conventional T cells (TCD4 or Tconv), Treg ratio, and LGALS9 expression were analyzed by immunohistochemistry (IHC) and cytometry in blood and pancreas of K-rasLSL.G12D/+;Pdx-1-Cre (KC) and KrasWildType (WT);Pdx1-Cre (WT) mice aged 4-13 months. Pancreatic intraepithelial neoplasm (PanIN) progression and grade were quantified using FIJI software and validated by pathologists. The anti-galectin-9 mAb was validated for its use in mice on isolated murine C57BL/6 Treg by immunofluorescence staining and cytometry. Its specificity and functionality were validated in proliferation assays on rLGALS9-immunosuppressed murine Tconv and in suppression assays between murine Treg and Tconv. Finally, 2-month-old KC mice were treated with anti-LGALS9 and compared to WT mice for peripheral and infiltrating TCD4, Treg, and PanIN progression. Results: IHC and cytometry revealed a significant increase in LGALS9 expression and Treg levels in the blood and pancreas of KC mice proportional to the stages of precancerous lesions. Although present in WT mice, LGALS9 is expressed at a basal level with low and restricted expression that increases slightly over time, while Treg cells are few in number in their circulation and even absent from the pancreas over time. Using our anti-LGALS9 mAb in mice, it is shown that (i) murine Treg express LGALS9, (ii) the mAb could target and inhibit recombinant murine LGALS9, and (iii) neutralize murine Treg suppressive activity. Finally, the anti-LGALS9 mAb in KC mice reduced (i) LGALS9 expression in pancreatic cancer cells, (ii) the Treg ratio, and (iii) the total surface area and grade of PanIN. Conclusion: We demonstrate for the first time that an anti-LGALS9 antibody, by specifically targeting endogenous LGALS9 tumor and exogenous LGALS9 produced by Treg, was able to limit the progression of pancreatic neoplastic lesions in mice, opening up new prospects for its use as an immunotherapeutic tool in PDAC. [ABSTRACT FROM AUTHOR]

Published
2023
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15. Expression and function of Olfr78 and Olfr558 in the mouse gastrointestinal tract

Author

Garcia, Marie-Isabelle, Parmentier, Marc, Moreno, Christophe, Pirson, Isabelle, Van Keymeulen, Alexandra, Laurent, Patrick, Depoortere, Inge, Van Seuningen, Isabelle IVS, Dinsart, Gilles, Garcia, Marie-Isabelle, Parmentier, Marc, Moreno, Christophe, Pirson, Isabelle, Van Keymeulen, Alexandra, Laurent, Patrick, Depoortere, Inge, Van Seuningen, Isabelle IVS, and Dinsart, Gilles

Abstract

Les récepteurs olfactifs (OR) constituent la plus grande famille de récepteurs couplés aux protéines G (RCPG). L'intérêt croissant pour l'étude de ces récepteurs en dehors de la sphère olfactive a apporté des informations concernant l'expression des OR et leurs fonctions potentielles dans plusieurs tissus, tels que la peau, le cœur ou l'intestin. Au départ de ce projet, deux OR particuliers, nommés OR51E1/Olfr558 et OR51E2/Olfr78 (orthologues humain/souris), avaient été montrés comme étant exprimés dans certains sous-types de cellules entéroendocrines (EEC) de l’intestin. Les EEC jouent un rôle majeur dans la régulation du métabolisme global et de l’homéostasie intestinale grâce à la sécrétion d’hormones telles que GLP-1, PYY, ou encore la sérotonine aussi nommée 5-Hydroxytryptamine (5-HT). Il a été proposé que ces deux ORs, répondant aux acides gras à chaîne courte produits massivement par le microbiote intestinal, seraient impliqués dans la sécrétion des hormones EEC. Afin de mieux comprendre le rôle biologique potentiel de ces deux ORs dans l’intestin murin, nous avons d’abord étudié le profil d'expression complet de ces récepteurs le long du tractus digestif, en particulier celui de Olfr78. Nous avons montré que leur expression était principalement restreinte aux cellules épithéliales et mésenchymateuses du côlon. Ensuite, grâce à l’utilisation de la lignée murine transgénique rapportrice Olfr78-GFP dite « knock-in/knock-out » pour le récepteur Olfr78, nous avons pu étudier le profil transcriptomique des cellules épithéliales coliques exprimant Olfr78 et avons montré qu'il s’agit de cellules neuroendocrines de deux sous-types de EEC :les cellules L capables de produire du GLP-1 et du PYY et les cellules entérochromaffines (EC) sécrétant 5-HT. Ces dernières cellules sont enrichies en marqueurs présynaptiques et coexpriment l’OR Olfr558. En outre, nous avons démontré que la différenciation terminale des cellules EC, mais pas celle des cellules L, était déficiente, Doctorat en Sciences biomédicales et pharmaceutiques (Médecine), info:eu-repo/semantics/nonPublished

Published
2023

16. Metabolism of pancreatic neuroendocrine tumors: what can omics tell us?

Author

Jannin, Arnaud, Dessein, Anne-Frédérique, Do Cao, Christine, Vantyghem, Marie-Christine, Chevalier, Benjamin, Van Seuningen, Isabelle, Jonckheere, Nicolas, and Coppin, Lucie

Subjects
PANCREATIC tumors, NEUROENDOCRINE tumors, AMINO acid metabolism, KREBS cycle, GENE expression profiling, METABOLISM
Abstract

Introduction: Reprogramming of cellular metabolism is now a hallmark of tumorigenesis. In recent years, research on pancreatic neuroendocrine tumors (pNETs) has focused on genetic and epigenetic modifications and related signaling pathways, but few studies have been devoted to characterizing the metabolic profile of these tumors. In this review, we thoroughly investigate the metabolic pathways in pNETs by analyzing the transcriptomic and metabolomic data available in the literature. Methodology: We retrieved and downloaded gene expression profiles from all publicly available gene set enrichments (GSE43797, GSE73338, and GSE117851) to compare the differences in expressed genes based on both the stage and MEN1 mutational status. In addition, we conducted a systematic review of metabolomic data in NETs. Results: By combining transcriptomic and metabolomic approaches, we have identified a distinctive metabolism in pNETs compared with controls without pNETs. Our analysis showed dysregulations in the one-carbon, glutathione, and polyamine metabolisms, fatty acid biosynthesis, and branched-chain amino acid catabolism, which supply the tricarboxylic acid cycle. These targets are implicated in pNET cell proliferation and metastasis and could also have a prognostic impact. When analyzing the profiles of patients with or without metastasis, or with or without MEN1 mutation, we observed only a few differences due to the scarcity of published clinical data in the existing research. Consequently, further studies are now necessary to validate our data and investigate these potential targets as biomarkers or therapeutic solutions, with a specific focus on pNETs. [ABSTRACT FROM AUTHOR]

Published
2023
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21. Hemidesmosome integrity protects the colon against colitis and colorectal cancer

Author

De Arcangelis, Adèle, Hamade, Hussein, Alpy, Fabien, Normand, Sylvain, Bruyère, Emilie, Lefebvre, Olivier, Méchine-Neuville, Agnès, Siebert, Stéphanie, Pfister, Véronique, Lepage, Patricia, Laquerriere, Patrice, Dembele, Doulaye, Delanoye-Crespin, Anne, Rodius, Sophie, Robine, Sylvie, Kedinger, Michèle, Van Seuningen, Isabelle, Simon-Assmann, Patricia, Chamaillard, Mathias, Labouesse, Michel, and Georges-Labouesse, Elisabeth

Published
2017
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24. Neurotrophins promotes brain metastasis of triple negative breast cancer through Src kinase family activation

Author

Cicero, Julien, Trouvilliez, Sarah, Palma, Martine, Ternier, Gaetan, Decoster, Laurine, Barrois, Nicolas, Dehouck, Lucie, Happernegg, Eloise, Bourette, Roland, Adriaenssens, Eric, Lagadec, Chann, Tarhan, Mehmet, Collard, Dominique, Souguir, Zied, Vandenhaute, Elodie, Maubon, Grégory, Maubon, Nathalie, SIPIETER, FRANCOIS, Sipieter, François, Borghi, Nicolas, Giacobini, Paolo, Prevost, Vincent, Gosselet, Fabien, Le Bourhis, Xuefen, van Seuningen, Isabelle, Mysiorek, Caroline, Toillon, Robert-Alain, IEMN, Collection, Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 (CANTHER), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de la Barrière Hémato-Encéphalique (LBHE), Université d'Artois (UA), Centre Régional de Lutte contre le Cancer Oscar Lambret [Lille] (UNICANCER/Lille), Université de Lille-UNICANCER, CHU Lille, Lille Neurosciences & Cognition - U 1172 (LilNCog), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Plateformes Lilloises en Biologie et Santé - UAR 2014 - US 41 (PLBS), Institut d’Électronique, de Microélectronique et de Nanotechnologie - UMR 8520 (IEMN), Centrale Lille-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-JUNIA (JUNIA), Université catholique de Lille (UCL)-Université catholique de Lille (UCL), Bio-Micro-Electro-Mechanical Systems - IEMN (BIOMEMS - IEMN), Université catholique de Lille (UCL)-Université catholique de Lille (UCL)-Centrale Lille-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-JUNIA (JUNIA), JUNIA (JUNIA), Université catholique de Lille (UCL), Laboratory for Integrated Micro Mechatronics Systems (LIMMS), The University of Tokyo (UTokyo)-Centre National de la Recherche Scientifique (CNRS), HCS-Pharma Loos [Lille] (HCS-PL), Institut Jacques Monod (IJM (UMR_7592)), Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), and Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
[SPI]Engineering Sciences [physics], [SPI] Engineering Sciences [physics]
Abstract

ORAL; International audience; With nearly 2.3 million cases diagnosed worldwide each year and an estimated 685 000 deaths by 2020, breast cancer is the leading cause of cancer-related death in women. Brain metastases cause severe cognitive complications that severely impair quality of life. In TN breast cancer, the prognosis for brain metastases is particularly poor with a median survival of no more than 6 months. It is therefore crucial to know the molecular actors that promote the metastatic dissemination of triple negative breast cancer to the brain but also to prevent the proliferation of brain micrometastases that can cause fatal recurrences. In order to recapitulate several final stages of brain metastasis, we used both human Blood- Brain-Barrier in vitro model, human organotypic 3D extracellular in vitro matrix, mice brain slices organotypic ex vivo culture and in vivo mice xenograft. These models are coupled with single cell, 3D and real time imaging techniques, including FRET biosensing. This unique experimental approach allows us to study the involvement of signaling pathways in these different biological processes. Using this innovative method, we have identified that inhibition neurotrophins receptor leads to a decrease in the activity of the underlying signaling pathways and consequently to a decrease in the ability of breast cancer cells to pass through the BBB, to grow and to colonize the brain parenchyma.

Published
2022

26. Analysis of the proximal promoter of the human colon-specific B4GALNT2 (Sda synthase) gene: B4GALNT2 is transcriptionally regulated by ETS1

Author

Wavelet-Vermuse, Cindy, Groux-Degroote, Sophie, Vicogne, Dorothée, Cogez, Virginie, Venturi, Giulia, Trinchera, Marco, Brysbaert, Guillaume, Krzewinski-Recchi, Marie-Ange, Bachir, Elsa Hadj, Schulz, Céline, Vincent, Audrey, Van Seuningen, Isabelle, Harduin-Lepers, Anne, Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 (CANTHER), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Unité de Glycobiologie Structurale et Fonctionnelle (UGSF), Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Alma Mater Studiorum Università di Bologna [Bologna] (UNIBO), Universitá degli Studi dell’Insubria, This work was supported in part by the Centre National de la Recherche Scientifique (CNRS), the University of Lille. La Ligue contre le cancer (2016) and the Agence Nationale de la Recherche (ANR) financial support (ANR-2010-BLAN-120401) are acknowledged., ANR-10-BLAN-1204,GALFISH,Régulation moléculaire et cellulaire de la beta1,4-GalNAcT-II dans les états physiologiques et pathologiques (cancers gastrointestinaux)(2010), Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER], Unité de Glycobiologie Structurale et Fonctionnelle - UMR 8576 (UGSF), Université de Lille-Centre National de la Recherche Scientifique (CNRS), Universitá degli Studi dell’Insubria = University of Insubria [Varese] (Uninsubria), Harduin-Lepers, Anne, and BLANC - Régulation moléculaire et cellulaire de la beta1,4-GalNAcT-II dans les états physiologiques et pathologiques (cancers gastrointestinaux) - - GALFISH2010 - ANR-10-BLAN-1204 - BLANC - VALID

Subjects
Transcriptional regulation, ETS1, Colon, [SDV]Life Sciences [q-bio], B4GALNT2, Core promoter, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, ComputingMilieux_MISCELLANEOUS
Abstract

International audience; Background: The Sda antigen and corresponding biosynthetic enzyme B4GALNT2 are primarily expressed in normal colonic mucosa and are down-regulated to a variable degree in colon cancer tissues. Although their expression profile is well studied, little is known about the underlying regulatory mechanisms. Methods: To clarify the molecular basis of Sda expression in the human gastrointestinal tract, we investigated the transcriptional regulation of the human B4GALNT2 gene. The proximal promoter region was delineated using luciferase assays and essential trans-acting factors were identified through transient overexpression and silencing of several transcription factors. Results: A short cis-regulatory region restricted to the −72 to +12 area upstream of the B4GALNT2 short-type transcript variant contained the essential promoter activity that drives the expression of the human B4GALNT2 regardless of the cell type. We further showed that B4GALNT2 transcriptional activation mostly requires ETS1 and to a lesser extent SP1. Conclusions: Results presented herein are expected to provide clues to better understand B4GALNT2 regulatory mechanisms.

Published
2021

32. TRPM7 Modulates Human Pancreatic Stellate Cell Activation.

Author

Auwercx, Julie, Kischel, Philippe, Lefebvre, Thibaut, Jonckheere, Nicolas, Vanlaeys, Alison, Guénin, Stéphanie, Radoslavova, Silviya, Van Seuningen, Isabelle, Ouadid-Ahidouch, Halima, Kocher, Hemant M., Dhennin-Duthille, Isabelle, and Gautier, Mathieu

Subjects
PANCREATIC duct, LIVER cells, FIBROBLASTS, PANCREATIC diseases, PI3K/AKT pathway, CELL cycle
Abstract

Pancreatic diseases, such as pancreatitis or pancreatic ductal adenocarcinoma, are characterized by the presence of activated pancreatic stellate cells (PSCs). These cells represent key actors in the tumor stroma, as they actively participate in disease development and progression: reprograming these PSCs into a quiescent phenotype has even been proposed as a promising strategy for restoring the hallmarks of a healthy pancreas. Since TRPM7 channels have been shown to regulate hepatic stellate cells proliferation and survival, we aimed to study the role of these magnesium channels in PSC activation and proliferation. PS-1 cells (isolated from a healthy pancreas) were used as a model of healthy PSCs: quiescence or activation were induced using all-trans retinoic acid or conditioned media of pancreatic cancer cells, respectively. The role of TRPM7 was studied by RNA silencing or by pharmacological inhibition. TRPM7 expression was found to be correlated with the activation status of PS-1 cells. TRPM7 expression was able to regulate proliferation through modulation of cell cycle regulators and most importantly p53, via the PI3K/Akt pathway, in a magnesium-dependent manner. Finally, the analysis of TCGA database showed the overexpression of TRPM7 in cancer-associated fibroblasts. Taken together, we provide strong evidences that TRPM7 can be considered as a marker of activated PSCs. [ABSTRACT FROM AUTHOR]

Published
2022
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45. Epigenetic Regulation by lncRNAs: An Overview Focused on UCA1 in Colorectal Cancer

Author

Neve, Bernadette, Jonckheere, Nicolas, Vincent, Audrey, Van Seuningen, Isabelle, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U1172 Inserm - U837 (JPArc), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Lille Nord de France (COMUE)-Université de Lille, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 (JPArc), Université Lille Nord de France (COMUE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, and Jonckheere, Nicolas

Subjects
[SDV.CAN] Life Sciences [q-bio]/Cancer, lncRNA Urothelial Cancer Associated 1 (UCA1), [SDV]Life Sciences [q-bio], competing endogenous RNAs (ceRNA), [SDV.CAN]Life Sciences [q-bio]/Cancer, Review, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, lcsh:RC254-282, colorectal cancer (CRC), long non-coding RNA (lncRNA), ComputingMilieux_MISCELLANEOUS
Abstract

International audience; Colorectal cancers have become the second leading cause of cancer-related deaths. In particular, acquired chemoresistance and metastatic lesions occurring in colorectal cancer are a major challenge for chemotherapy treatment. Accumulating evidence shows that long non-coding (lncRNAs) are involved in the initiation, progression, and metastasis of cancer. We here discuss the epigenetic mechanisms through which lncRNAs regulate gene expression in cancer cells. In the second part of this review, we focus on the role of lncRNA Urothelial Cancer Associated 1 (UCA1) to integrate research in different types of cancer in order to decipher its putative function and mechanism of regulation in colorectal cancer cells. UCA1 is highly expressed in cancer cells and mediates transcriptional regulation on an epigenetic level through the interaction with chromatin modifiers, by direct regulation via chromatin looping and/or by sponging the action of a diversity of miRNAs. Furthermore, we discuss the role of UCA1 in the regulation of cell cycle progression and its relation to chemoresistance in colorectal cancer cells.

Published
2018

47. Description of an IL-1-responsive kinase that phosphorylates the K protein. Enhancement of phosphorylation by selective DNA and RNA motifs

Author

Seuningen, Isabelle van, Ostrowski, Jerzy, and Bomsztyk, Karol

Subjects
Proteins -- Research, Phosphorylation -- Analysis, Nucleic acids -- Analysis, Biological sciences, Chemistry
Abstract

The phosphorylation of K protein is mediated by related DNA and RNA sequences and it forms a complex with interleukin-1 (IL-1). The K protein regulates the gene expression. The IL-1 kinase activity associated with K protein is reduced on phosphatase treatment.

Published
1995

50. MOESM5 of Integrative analysis of the cancer genome atlas and cancer cell lines encyclopedia large-scale genomic databases: MUC4/MUC16/MUC20 signature is associated with poor survival in human carcinomas

Author

Jonckheere, Nicolas and Seuningen, Isabelle Van

Subjects
sense organs
Abstract

Additional file 5: Figure S4. Correlation of MUC4 expression and copy numbers of genes correlated with MUC4. The top genes were defined as genes harboring Pearsonâ s correlation higher than 0.5 with MUC4 expression. MUC4 mRNA expression and log2 copy number of ADGRF1, LCN2, MUC20, C1ORF116, STEAP4, SCEL, MUC16 were extracted using ( https://portals.broadinstitute.org/ccle ).

Published
2018
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