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Your search keyword '"MESH: Colonic Neoplasms"' showing total 5 results
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5 results on '"MESH: Colonic Neoplasms"'

1. A ligand-insensitive UNC5B splicing isoform regulates angiogenesis by promoting apoptosis

Author

Alex Pezzotta, Anna Pistocchi, Patrick Mehlen, Andrea Paradisi, Anna Di Matteo, Federico Forneris, Daniele Campolungo, Costanza Giampietro, Elisa Belloni, Gianluca Deflorian, Nina Volf, Antonella Chiapparino, Michael Rehman, William Vermi, Maria Paola Paronetto, Mattia Bugatti, Davide Pradella, Claudia Ghigna, Anne Eichmann, Matteo Campioni, Serena Zacchigna, Luigi Scietti, Paradisi, Andrea, Consiglio Nazionale delle Ricerche (CNR), Università degli Studi di Pavia = University of Pavia (UNIPV), IFOM, Istituto FIRC di Oncologia Molecolare (IFOM), Università degli Studi di Milano = University of Milan (UNIMI), San Raffaele Scientific Institute, Vita-Salute San Raffaele University and Center for Translational Genomics and Bioinformatics, 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-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Développement Cancer et Thérapies Ciblées [Lyon] (LabEx DEVweCAN), Université de Lyon, Centre Léon Bérard [Lyon], University of Brescia, Washington University School of Medicine in St. Louis, Washington University in Saint Louis (WUSTL), Heidelberg University, Swiss Federal Laboratories for Materials Science and Technology [Dübendorf] (EMPA), International Centre for Genetic Engineering and Biotechnology (ICGEB) (Trieste), Yale School of Medicine [New Haven, Connecticut] (YSM), Università degli studi di Trieste = University of Trieste, IRCCS Ospedale Pediatrico Bambino Gesù [Roma], University of Rome 'Foro Italico', Paris-Centre de Recherche Cardiovasculaire (PARCC (UMR_S 970/ U970)), 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)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Pradella, D., Deflorian, G., Pezzotta, A., Di Matteo, A., Belloni, E., Campolungo, D., Paradisi, A., Bugatti, M., Vermi, W., Campioni, M., Chiapparino, A., Scietti, L., Forneris, F., Giampietro, C., Volf, N., Rehman, M., Zacchigna, S., Paronetto, M. P., Pistocchi, A., Eichmann, A., Mehlen, P., Ghigna, C., University of Pavia, University of Milan, Yale University School of Medicine, University of Trieste, and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP)

Subjects
Netrin Receptor, Angiogenesis, Regulator, General Physics and Astronomy, Apoptosis, RNA-binding protein, RNA-Binding Protein, 0302 clinical medicine, Netrin, Morphogenesis, RNA Isoforms, MESH: Animals, MESH: Endothelial Cells, MESH: Nerve Tissue Proteins, Zebrafish, Colonic Neoplasm, Endothelial Cell, 0303 health sciences, Multidisciplinary, Neovascularization, Pathologic, Chemistry, MESH: Alternative Splicing, RNA-Binding Proteins, RNA Isoform, Netrin-1, Cell biology, MESH: Survival Analysis, 030220 oncology & carcinogenesis, embryonic structures, Colonic Neoplasms, RNA splicing, Survival Analysi, Netrin Receptors, Human, Gene isoform, animal structures, Blood Vessel, Science, Nerve Tissue Proteins, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Article, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, Neuro-Oncological Ventral Antigen, Morphogenesi, Animals, Humans, Alternative Splicing, Blood Vessels, Endothelial Cells, Survival Analysis, MESH: Zebrafish, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, Neovascularization, 030304 developmental biology, Pathologic, MESH: Colonic Neoplasms, MESH: Humans, Animal, MESH: Apoptosis, fungi, Alternative splicing, MESH: Blood Vessels, General Chemistry, MESH: Netrin Receptors, MESH: RNA Isoforms, MESH: Morphogenesis, Exon skipping, MESH: RNA-Binding Proteins, nervous system, MESH: Netrin-1, Nerve Tissue Protein, MESH: Neovascularization, Pathologic, Tumour angiogenesis
Abstract

The Netrin-1 receptor UNC5B is an axon guidance regulator that is also expressed in endothelial cells (ECs), where it finely controls developmental and tumor angiogenesis. In the absence of Netrin-1, UNC5B induces apoptosis that is blocked upon Netrin-1 binding. Here, we identify an UNC5B splicing isoform (called UNC5B-Δ8) expressed exclusively by ECs and generated through exon skipping by NOVA2, an alternative splicing factor regulating vascular development. We show that UNC5B-Δ8 is a constitutively pro-apoptotic splicing isoform insensitive to Netrin-1 and required for specific blood vessel development in an apoptosis-dependent manner. Like NOVA2, UNC5B-Δ8 is aberrantly expressed in colon cancer vasculature where its expression correlates with tumor angiogenesis and poor patient outcome. Collectively, our data identify a mechanism controlling UNC5B’s necessary apoptotic function in ECs and suggest that the NOVA2/UNC5B circuit represents a post-transcriptional pathway regulating angiogenesis., Nature Communications, 12, ISSN:2041-1723

Published
2021
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2. Metformin regulates global DNA methylation via mitochondrial one-carbon metabolism

Author

Jorge Joven, Sara Verdura, Salvador Fernández-Arroyo, Elisa Blanco-González, Javier A. Menendez, Maria Montes-Bayón, Jan Stursa, R Á-F García, Elisabet Cuyàs, Benoit Viollet, Lukas Werner, Jiri Neuzil, Program Against Cancer Therapeutic Resistance/Metabolism & Cancer Group [Catalonia, Spain] (ProCURE), Catalan Institute of Oncology-Girona (ICO-Girona), Girona Biomedical Research Institute [Girona, Spain] (IDIBGI), Unitat de Recerca Biomedica [Reus, Spain], Hospital Universitari de Sant Joan [Reus, Spain]-Rovira i Virgili University [Reus, Spain] (IISPV), The Campus of International Excellence Southern Catalonia [Tarragona, Spain], Department of Physical and Analytical Chemistry oviedo [Oviedo, Spain] ( Faculty of Chemistry), University of Oviedo, Institute of Chemical Technology [Prague, Czech Republic], Institute of Biotechnology [Prague-West, Czech Republic], Czech Academy of Sciences [Prague] (CAS), [Institut Cochin] Département Endocrinologie, métabolisme, diabète (EMD) (EMD), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-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 National de la Recherche Scientifique (CNRS), School of Medical Science [Queensland, Australia], Griffith University [Brisbane], and Viollet, Benoit

Subjects
0301 basic medicine, S-Adenosylmethionine, Cancer Research, Methyltransferase, AMP-Activated Protein Kinases, Mitochondrion, MESH: Metformin, Mice, MESH: DNA Methylation, Tumor Cells, Cultured, MESH: Animals, MESH: AMP-Activated Protein Kinases, [SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Regulation of gene expression, MESH: Electron Transport Complex I, Biguanide, MESH: Follow-Up Studies, MESH: Gene Expression Regulation, Neoplastic, Methylation, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, S-Adenosylhomocysteine, Metformin, Mitochondria, Cell biology, Gene Expression Regulation, Neoplastic, Colonic Neoplasms, DNA methylation, Female, MESH: Biomarkers, Tumor, Reprogramming, medicine.drug, MESH: S-Adenosylhomocysteine, MESH: Mitochondria, medicine.drug_class, MESH: Carbon, Breast Neoplasms, Biology, 03 medical and health sciences, MESH: Hypoglycemic Agents, Biomarkers, Tumor, Genetics, medicine, Animals, Humans, Hypoglycemic Agents, MESH: Tumor Cells, Cultured, MESH: Mice, Molecular Biology, MESH: Genome, Human, MESH: Colonic Neoplasms, MESH: Humans, Electron Transport Complex I, Genome, Human, MESH: S-Adenosylmethionine, DNA Methylation, Carbon, 030104 developmental biology, MESH: Female, MESH: Breast Neoplasms, Follow-Up Studies
Abstract

International audience; The anti-diabetic biguanide metformin may exert health-promoting effects via metabolic regulation of the epigenome. Here we show that metformin promotes global DNA methylation in non-cancerous, cancer-prone and metastatic cancer cells by decreasing S-adenosylhomocysteine (SAH), a strong feedback inhibitor of S-adenosylmethionine (SAM)-dependent DNA methyltransferases, while promoting the accumulation of SAM, the universal methyl donor for cellular methylation. Using metformin and a mitochondria/complex I (mCI)-targeted analog of metformin (norMitoMet) in experimental pairs of wild-type and AMP-activated protein kinase (AMPK)-, serine hydroxymethyltransferase 2 (SHMT2)- and mCI-null cells, we provide evidence that metformin increases the SAM:SAH ratio-related methylation capacity by targeting the coupling between serine mitochondrial one-carbon flux and CI activity. By increasing the contribution of one-carbon units to the SAM from folate stores while decreasing SAH in response to AMPK-sensed energetic crisis, metformin can operate as a metabolo-epigenetic regulator capable of reprogramming one of the key conduits linking cellular metabolism to the DNA methylation machinery.

Published
2017
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3. The tumor suppressor activity induced by adenovirus-mediated BRCA1 overexpression is not restricted to breast cancers

Author

Voahangy Randrianarison, Michel Perricaudet, Jean Feunteun, N Elie, Paule Opolon, Nicolas Foray, Didier Marot, S Brailly-Tabard, Elisabeth Connault, Matrice extracellulaire et régulations cellulaires (MERC), Université de Reims Champagne-Ardenne (URCA)-Centre National de la Recherche Scientifique (CNRS), Vectorologie et transfert de gènes (VTG / UMR8121), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Centre National de la Recherche Scientifique (CNRS), Génétique oncologique (GO - UMR 8125), Rayonnement Synchrotron et Recherche Medicale (RSRM), Université Joseph Fourier - Grenoble 1 (UJF)-European Synchrotron Radiation Facility (ESRF)-Institut National de la Santé et de la Recherche Médicale (INSERM), and European Synchrotron Radiation Facility (ESRF)-Université Joseph Fourier - Grenoble 1 (UJF)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Male, Lung Neoplasms, Angiogenesis, Genes, BRCA1, Apoptosis, MESH: Cell Cycle, Injections, Intralesional, Retinoblastoma Protein, Mice, 0302 clinical medicine, MESH: Genetic Vectors, Genes, Tumor Suppressor, MESH: Animals, 0303 health sciences, Cell Cycle, MESH: Genetic Predisposition to Disease, MESH: Adenoviridae, MESH: Gene Expression Regulation, Neoplastic, Cell cycle, 3. Good health, Gene Expression Regulation, Neoplastic, 030220 oncology & carcinogenesis, Colonic Neoplasms, Molecular Medicine, Female, HT29 Cells, G1 phase, MESH: Cell Line, Tumor, Tumor suppressor gene, Genetic Vectors, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, MESH: G1 Phase, Adenoviridae, 03 medical and health sciences, Breast cancer, Cell Line, Tumor, Genetics, medicine, Animals, Humans, Genetic Predisposition to Disease, E2F, Molecular Biology, 030304 developmental biology, MESH: Colonic Neoplasms, MESH: HT29 Ce, Cell growth, MESH: Apoptosis, G1 Phase, Genetic Therapy, MESH: Genes, Tumor Suppressor, medicine.disease, Androgen receptor, Cancer research, MESH: Gene Therapy, MESH: Genes, BRCA1, MESH: Female, Neoplasm Transplantation
Abstract

International audience; The BRCA1 (breast cancer 1) breast cancer susceptibility gene is recognized as responsible for most familial breast and ovarian cancers and is suggested to be a tissue-specific tumor suppressor gene. In this report, we investigated the tissue specificity of tumor inhibitory activities induced by a recombinant adenovirus coding for wild-type BRCA1 (wtAdBRCA1). We demonstrated a pronounced in vitro antiproliferative effect on H1299 lung and HT29 colon cells upon infection with AdBRCA1. We describe a prolonged G1 cell cycle arrest associated with a decrease in the hyperphosphorylated form of Rb, suggesting that the Rb/E2F pathway is implicated in BRCA1-induced cell growth arrest. We also observed a significant antitumor effect in these pre-established subcutaneous tumors after in situ delivery of AdBRCA1, although these two tumors do not express wt p53, and also estrogen alpha and beta, progesterone and androgen receptors. Moreover, BRCA1 can induce a strong prolonged cell cycle arrest and apoptotic cell death but no significant antiangiogenic effect in H1299 tumors. Finally, our data indicate that intratumor administration of wtAdBRCA1 significantly inhibits growth of lung and colon steroid hormone-independent tumors.

Published
2005
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4. Increase in intracellular PGE2 induces apoptosis in Bax-expressing colon cancer cell

Author

Christophe Olivier, Christophe Braud, François M. Vallette, François Pedelaborde, Lisenn Lalier, Jean Menanteau, Département de Biologie Oncologique, Centre de Lutte Contre le Cancer René Gauducheau, Centre de Recherche en Cancérologie Nantes-Angers (CRCNA), Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM)-Hôtel-Dieu de Nantes-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital Laennec-Centre National de la Recherche Scientifique (CNRS)-Faculté de Médecine d'Angers-Centre hospitalier universitaire de Nantes (CHU Nantes), Laboratoire de Toxicologie, Université de Nantes (UN), and BMC, Ed.

Subjects
Cancer Research, MESH: Cyclooxygenase 2 Inhibitors, Colorectal cancer, Intracellular Space, Apoptosis, MESH: Microinjections, 0302 clinical medicine, Prostaglandin-E Synthases, bcl-2-Associated X Protein, 0303 health sciences, biology, MESH: Dinoprostone, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, 3. Good health, Intramolecular Oxidoreductases, Blot, MESH: Cell Survival, Oncology, 030220 oncology & carcinogenesis, Colonic Neoplasms, MESH: Intracellular Space, lipids (amino acids, peptides, and proteins), MESH: Cyclooxygenase 2, Stem cell, Intracellular, Research Article, MESH: Cell Line, Tumor, Microinjections, Cell Survival, MESH: HCT116 Cells, Blotting, Western, [SDV.CAN]Life Sciences [q-bio]/Cancer, lcsh:RC254-282, Dinoprostone, 03 medical and health sciences, Bcl-2-associated X protein, [SDV.CAN] Life Sciences [q-bio]/Cancer, Cell Line, Tumor, Genetics, medicine, Humans, MESH: Blotting, Western, MESH: bcl-2-Associated X Protein, 030304 developmental biology, MESH: Colonic Neoplasms, MESH: Humans, Cyclooxygenase 2 Inhibitors, business.industry, MESH: Apoptosis, Cancer, HCT116 Cells, medicine.disease, MESH: Intramolecular Oxidoreductases, digestive system diseases, Cyclooxygenase 2, Cell culture, Immunology, Cancer research, biology.protein, business
Abstract

Background NSAIDs exhibit protective properties towards some cancers, especially colon cancer. Yet, it is not clear how they play their protective role. PGE2 is generally shown as the only target of the NSAIDs anticancerous activity. However, PGE2 known targets become more and more manifold, considering both the molecular pathways involved and the target cells in the tumour. The role of PGE2 in tumour progression thus appears complex and multipurpose. Methods To gain understanding into the role of PGE2 in colon cancer, we focused on the activity of PGE2 in apoptosis in colon cancer cell lines. Results We observed that an increase in intracellular PGE2 induced an apoptotic cell death, which was dependent on the expression of the proapoptotic protein Bax. This increase was induced by increasing PGE2 intracellular concentration, either by PGE2 microinjection or by the pharmacological inhibition of PGE2 exportation and enzymatic degradation. Conclusions We present here a new sight onto PGE2 in colon cancer cells opening the way to a new prospective therapeutic strategy in cancer, alternative to NSAIDs.

Published
2011
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5. Reverse transcription-quantitative polymerase chain reaction: description of a RIN-based algorithm for accurate data normalization

Author

Marc Ychou, Florence Boissière-Michot, Evelyne Lopez-Crapez, Frédéric Bibeau, Dominic Cellier, Alexandre Ho-Pun-Cheung, Eric Assenat, Caroline Bascoul-Mollevi, Merck Santé - Lyon, Merck & Co. Inc, Département d'oncologie Médicale, CRLCC Val d'Aurelle - Paul Lamarque, Institut de recherche en cancérologie de Montpellier (IRCM - U896 Inserm - UM1), CRLCC Val d'Aurelle - Paul Lamarque-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 1 (UM1), Laboratoire d'anatomo-pathologie, Université Montpellier 1 (UM1)-CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), and Le Ster, Yves

Subjects
[SDV.BIO]Life Sciences [q-bio]/Biotechnology, Biopsy, RNA Stability, Statistics as Topic, MESH: Biopsy, 0302 clinical medicine, MESH: Reverse Transcriptase Polymerase Chain Reaction, Gene expression, [INFO.INFO-BT]Computer Science [cs]/Biotechnology, 0303 health sciences, lcsh:Cytology, Reverse Transcriptase Polymerase Chain Reaction, Methodology Article, MESH: RNA Stability, MESH: Gene Expression Regulation, 3. Good health, MESH: Reproducibility of Results, Real-time polymerase chain reaction, 030220 oncology & carcinogenesis, Colonic Neoplasms, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Algorithm, Algorithms, Normalization (statistics), MESH: Cell Line, Tumor, lcsh:QH426-470, MESH: HCT116 Cells, Breast Neoplasms, MESH: Algorithms, Biology, Database normalization, 03 medical and health sciences, Cell Line, Tumor, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Humans, lcsh:QH573-671, Molecular Biology, MESH: Statistics as Topic, 030304 developmental biology, MESH: Colonic Neoplasms, Messenger RNA, MESH: Humans, Rectal Neoplasms, Reproducibility of Results, MESH: Rectal Neoplasms, RNA, HCT116 Cells, Reverse transcriptase, [SDV.BIO] Life Sciences [q-bio]/Biotechnology, lcsh:Genetics, [INFO.INFO-BT] Computer Science [cs]/Biotechnology, Gene Expression Regulation, MESH: Breast Neoplasms
Abstract

Background Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) is the gold standard technique for mRNA quantification, but appropriate normalization is required to obtain reliable data. Normalization to accurately quantitated RNA has been proposed as the most reliable method for in vivo biopsies. However, this approach does not correct differences in RNA integrity. Results In this study, we evaluated the effect of RNA degradation on the quantification of the relative expression of nine genes (18S, ACTB, ATUB, B2M, GAPDH, HPRT, POLR2L, PSMB6 and RPLP0) that cover a wide expression spectrum. Our results show that RNA degradation could introduce up to 100% error in gene expression measurements when RT-qPCR data were normalized to total RNA. To achieve greater resolution of small differences in transcript levels in degraded samples, we improved this normalization method by developing a corrective algorithm that compensates for the loss of RNA integrity. This approach allowed us to achieve higher accuracy, since the average error for quantitative measurements was reduced to 8%. Finally, we applied our normalization strategy to the quantification of EGFR, HER2 and HER3 in 104 rectal cancer biopsies. Taken together, our data show that normalization of gene expression measurements by taking into account also RNA degradation allows much more reliable sample comparison. Conclusion We developed a new normalization method of RT-qPCR data that compensates for loss of RNA integrity and therefore allows accurate gene expression quantification in human biopsies.

Published
2009
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