The Long Noncoding RNA SPRY4-IT1 Increases the Proliferation of Human Breast Cancer Cells by Upregulating ZNF703 Expression
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Mechanical Forces Induce an Asthma Gene Signature in Healthy Airway Epithelial Cells Ayşe Kılıç1,10, Asher Ameli1,2,10, Jin-Ah Park3,10, Alvin T
www.nature.com/scientificreports OPEN Mechanical forces induce an asthma gene signature in healthy airway epithelial cells Ayşe Kılıç1,10, Asher Ameli1,2,10, Jin-Ah Park3,10, Alvin T. Kho4, Kelan Tantisira1, Marc Santolini 1,5, Feixiong Cheng6,7,8, Jennifer A. Mitchel3, Maureen McGill3, Michael J. O’Sullivan3, Margherita De Marzio1,3, Amitabh Sharma1, Scott H. Randell9, Jefrey M. Drazen3, Jefrey J. Fredberg3 & Scott T. Weiss1,3* Bronchospasm compresses the bronchial epithelium, and this compressive stress has been implicated in asthma pathogenesis. However, the molecular mechanisms by which this compressive stress alters pathways relevant to disease are not well understood. Using air-liquid interface cultures of primary human bronchial epithelial cells derived from non-asthmatic donors and asthmatic donors, we applied a compressive stress and then used a network approach to map resulting changes in the molecular interactome. In cells from non-asthmatic donors, compression by itself was sufcient to induce infammatory, late repair, and fbrotic pathways. Remarkably, this molecular profle of non-asthmatic cells after compression recapitulated the profle of asthmatic cells before compression. Together, these results show that even in the absence of any infammatory stimulus, mechanical compression alone is sufcient to induce an asthma-like molecular signature. Bronchial epithelial cells (BECs) form a physical barrier that protects pulmonary airways from inhaled irritants and invading pathogens1,2. Moreover, environmental stimuli such as allergens, pollutants and viruses can induce constriction of the airways3 and thereby expose the bronchial epithelium to compressive mechanical stress. In BECs, this compressive stress induces structural, biophysical, as well as molecular changes4,5, that interact with nearby mesenchyme6 to cause epithelial layer unjamming1, shedding of soluble factors, production of matrix proteins, and activation matrix modifying enzymes, which then act to coordinate infammatory and remodeling processes4,7–10. -
Amplification of Chromosome 8 Genes in Lung Cancer Onur Baykara1, Burak Bakir1, Nur Buyru1, Kamil Kaynak2, Nejat Dalay3
Journal of Cancer 2015, Vol. 6 270 Ivyspring International Publisher Journal of Cancer 2015; 6(3): 270-275. doi: 10.7150/jca.10638 Research Paper Amplification of Chromosome 8 Genes in Lung Cancer Onur Baykara1, Burak Bakir1, Nur Buyru1, Kamil Kaynak2, Nejat Dalay3 1. Department of Medical Biology, Cerrahpasa Medical Faculty, Istanbul University, Turkey 2. Department of Chest Surgery, Cerrahpasa Medical Faculty, Istanbul University, Turkey 3. Department of Basic Oncology, I.U. Oncology Institute, Istanbul University, Turkey Corresponding author: Prof. Dr. Nejat Dalay, I.U.Oncology Institute, 34093 Capa, Istanbul, Turkey. e-mail : [email protected]; Phone : 90 542 2168861; Fax : 90 212 5348078 © 2015 Ivyspring International Publisher. Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. See http://ivyspring.com/terms for terms and conditions. Received: 2014.09.25; Accepted: 2014.12.18; Published: 2015.01.20 Abstract Chromosomal alterations are frequent events in lung carcinogenesis and usually display regions of focal amplification containing several overexpressed oncogenes. Although gains and losses of chromosomal loci have been reported copy number changes of the individual genes have not been analyzed in lung cancer. In this study 22 genes were analyzed by MLPA in tumors and matched normal tissue samples from 82 patients with non-small cell lung cancer. Gene amplifications were observed in 84% of the samples. Chromosome 8 was found to harbor the most frequent copy number alterations. The most frequently amplified genes were ZNF703, PRDM14 and MYC on chromosome 8 and the BIRC5 gene on chromosome 17. The frequency of deletions were much lower and the most frequently deleted gene was ADAM9. -
Sprouty Proteins, Masterminds of Receptor Tyrosine Kinase Signaling
CORE Metadata, citation and similar papers at core.ac.uk Provided by RERO DOC Digital Library Angiogenesis (2008) 11:53–62 DOI 10.1007/s10456-008-9089-1 ORIGINAL PAPER Sprouty proteins, masterminds of receptor tyrosine kinase signaling Miguel A. Cabrita Æ Gerhard Christofori Received: 14 December 2007 / Accepted: 7 January 2008 / Published online: 25 January 2008 Ó Springer Science+Business Media B.V. 2008 Abstract Angiogenesis relies on endothelial cells prop- Abbreviations erly processing signals from growth factors provided in Ang Angiopoietin both an autocrine and a paracrine manner. These mitogens c-Cbl Cellular homologue of Casitas B-lineage bind to their cognate receptor tyrosine kinases (RTKs) on lymphoma proto-oncogene product the cell surface, thereby activating a myriad of complex EGF Epidermal growth factor intracellular signaling pathways whose outputs include cell EGFR EGF receptor growth, migration, and morphogenesis. Understanding how eNOS Endothelial nitric oxide synthase these cascades are precisely controlled will provide insight ERK Extracellular signal-regulated kinase into physiological and pathological angiogenesis. The FGF Fibroblast growth factor Sprouty (Spry) family of proteins is a highly conserved FGFR FGF receptor group of negative feedback loop modulators of growth GDNF Glial-derived neurotrophic factor factor-mediated mitogen-activated protein kinase (MAPK) Grb2 Growth factor receptor-bound protein 2 activation originally described in Drosophila. There are HMVEC Human microvascular endothelial cell four mammalian orthologs (Spry1-4) whose modulation of Hrs Hepatocyte growth factor-regulated tyrosine RTK-induced signaling pathways is growth factor – and kinase substrate cell context – dependant. Endothelial cells are a group of HUVEC Human umbilical vein endothelial cell highly differentiated cell types necessary for defining the MAPK Mitogen-activated protein kinase mammalian vasculature. -
Graph Complexity Analysis Identifies an ETV5 Tumor-Specific Network in Human and Murine Low-Grade Glioma." Plos One.13,5
Washington University School of Medicine Digital Commons@Becker Open Access Publications 2018 Graph complexity analysis identifies na ETV5 tumor-specific network in human and murine low- grade glioma Yuan Pan Washington University School of Medicine in St. Louis Christina Duron Claremont Graduate University Erin C. Bush Claremont Graduate University Yu Ma Washington University School of Medicine in St. Louis Peter A. Sims Columbia University See next page for additional authors Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Pan, Yuan; Duron, Christina; Bush, Erin C.; Ma, Yu; Sims, Peter A.; Gutmann, David H.; Radunskaya, Ami; and Hardin, Johanna, ,"Graph complexity analysis identifies an ETV5 tumor-specific network in human and murine low-grade glioma." PLoS One.13,5. e0190001. (2018). https://digitalcommons.wustl.edu/open_access_pubs/6939 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. Authors Yuan Pan, Christina Duron, Erin C. Bush, Yu Ma, Peter A. Sims, David H. Gutmann, Ami Radunskaya, and Johanna Hardin This open access publication is available at Digital Commons@Becker: https://digitalcommons.wustl.edu/open_access_pubs/6939 RESEARCH ARTICLE Graph complexity analysis identifies an ETV5 tumor-specific network in human and murine low-grade glioma Yuan -
Transcriptomic and Epigenomic Characterization of the Developing Bat Wing
ARTICLES OPEN Transcriptomic and epigenomic characterization of the developing bat wing Walter L Eckalbar1,2,9, Stephen A Schlebusch3,9, Mandy K Mason3, Zoe Gill3, Ash V Parker3, Betty M Booker1,2, Sierra Nishizaki1,2, Christiane Muswamba-Nday3, Elizabeth Terhune4,5, Kimberly A Nevonen4, Nadja Makki1,2, Tara Friedrich2,6, Julia E VanderMeer1,2, Katherine S Pollard2,6,7, Lucia Carbone4,8, Jeff D Wall2,7, Nicola Illing3 & Nadav Ahituv1,2 Bats are the only mammals capable of powered flight, but little is known about the genetic determinants that shape their wings. Here we generated a genome for Miniopterus natalensis and performed RNA-seq and ChIP-seq (H3K27ac and H3K27me3) analyses on its developing forelimb and hindlimb autopods at sequential embryonic stages to decipher the molecular events that underlie bat wing development. Over 7,000 genes and several long noncoding RNAs, including Tbx5-as1 and Hottip, were differentially expressed between forelimb and hindlimb, and across different stages. ChIP-seq analysis identified thousands of regions that are differentially modified in forelimb and hindlimb. Comparative genomics found 2,796 bat-accelerated regions within H3K27ac peaks, several of which cluster near limb-associated genes. Pathway analyses highlighted multiple ribosomal proteins and known limb patterning signaling pathways as differentially regulated and implicated increased forelimb mesenchymal condensation in differential growth. In combination, our work outlines multiple genetic components that likely contribute to bat wing formation, providing insights into this morphological innovation. The order Chiroptera, commonly known as bats, is the only group of To characterize the genetic differences that underlie divergence in mammals to have evolved the capability of flight. -
Amplicons in Breast Cancers Analyzed by Multiplex Ligation-Dependent
Human Pathology (2019) 85,33–43 www.elsevier.com/locate/humpath Original contribution Amplicons in breast cancers analyzed by multiplex ligation-dependent probe amplification and fluorescence in situ hybridization☆,☆☆ Akishi Ooi MD, PhD a,b,⁎, Masafumi Inokuchi MD, PhD c, Shin-ichi Horike PhD d, Hiroko Kawashima MD, PhD e, Satoko Ishikawa MD, PhD c, Hiroko Ikeda MD, PhD b, Ritsuko Nakamura MD, PhD a, Takeru Oyama MD, PhD a, Yoh Dobashi MD, PhD f aDepartment of Molecular and Cellular Pathology, Kanazawa University, Ishikawa 920-8641, Japan bPathology Section, University Hospital, Kanazawa University, Ishikawa 920-8641, Japan cDepartment of Breast Oncology, Graduate School of Medical Science, Kanazawa University, Ishikawa 920-8641, Japan dAdvanced Science Research Center, Institute for Gene Research, Kanazawa University, Ishikawa 920-8641, Japan eSection of Breast Oncology, University Hospital, Kanazawa University, Ishikawa 920-8641, Japan fDepartment of Pathology, Saitama Medical Center, Jichi Medical University, Saitama, 330-8503, Japan Received 16 August 2018; revised 12 October 2018; accepted 18 October 2018 Keywords: Summary Gene amplification is a common event in breast cancer, and identifies actual and potential targets of Breast cancer; molecular therapy. The aim of the present study was to determine the amplification status of 22 genes that are Gene amplification; reportedly frequently amplified in breast cancers. An archive of 322 formalin-fixed and paraffin-embedded in- FISH; vasive breast cancer tissues were screened by multiple ligation-dependent probe amplification (MLPA) and a MLPA; total of 906 gene loci judged as ‘gain’ or ‘amplified’ was further confirmed to have been amplified based on Co-amplication fluorescence in situ hybridization (FISH). -
ZNF703 Overexpression May Act As an Oncogene In
Cancer Medicine Open Access ORIGINAL RESEARCH ZNF703 Overexpression may act as an oncogene in non-small cell lung cancer Onur Baykara1, Nejat Dalay2, Kamil Kaynak3 & Nur Buyru1 1Department of Medical Biology, Istanbul University Cerrahpasa Faculty of Medicine, Istanbul, Turkey 2Istanbul University Oncology Institute, Istanbul, Turkey 3Department of Chest Surgery, Istanbul University Cerrahpasa Faculty of Medicine, Istanbul, Turkey Keywords Abstract Akt/mTOR pathway, expression, NSCLC, ZNF703 Despite therapeutic advances, lung cancer remains one of the most common causes of cancer-related deaths worldwide. The ZNF703 gene has been identified Correspondence as the driver of the 8p11-12 region and its amplification or overexpression has Nur Buyru, Department of Medical Biology, been associated with several types of cancers. It has also been shown that ZNF703 Istanbul University Cerrahpasa Medical overexpression can activate the Akt/mTOR signaling pathway. The aim of our Faculty, Kat:6 Kocamustafapasa 34098, study was to investigate the role of the ZNF703 gene in association with Akt/mTOR Istanbul, Turkey. Tel: 90 505 5249471; Fax: 90 212 4143502; activation in non-small cell lung cancer (NSCLC). Expression levels in tumors E-mail: [email protected] and matched noncancerous tissue samples from 47 patients were analyzed by qRT-PCR and the Akt phosphorylation levels were investigated by Western Funding Information blotting. Our results show that ZNF703 is up-regulated in 63.4% of NSCLC This project has been supported by the tumor samples. Althogh the correlation did not reach a statistically significant Scientific and Technological Research Council level Akt phosphorylation was increased in tumor tissues expressing high levels of Turkey (TUBITAK) by project number of ZNF703. -
Levisticum Officinale Extract Triggers Apoptosis and Down-Regulates ZNF703 Gene Expression in Breast Cancer Cell Lines
Reports of Biochemistry & Molecular Biology Vol.8, No.2, July 2019 Original article www.RBMB.net Levisticum Officinale Extract Triggers Apoptosis and Down-Regulates ZNF703 Gene Expression in Breast Cancer Cell Lines Fatemeh Mollashahee-Kohkan1, 2, Ramin Saravani*1, 2, Tahereh Khalili2, Hamidreza Galavi1, 2, Saman Sargazi1 Abstract Background: Studies have shown that zinc finger protein 703 (ZNF703) is overexpressed in breast cancer. Levisticum (L.) officinale is a herbal plant with proven medical characteristics in traditional medicine. The purpose of the present study was to evaluate the effect of hydroalcoholic extract of L. officinale (HELO) on both estrogen receptor-positive (ER+) and -negative (ER-) cell lines (MCF-7 and MDA-MB-468, respectively). Methods: The anti-proliferative and apoptotic activities of HELO were investigated on both cell lines using MTT and flow-cytometry methods. Real-time PCR was employed to determinate the changes in mRNA expression of the ZNF703 gene. + - Results: The 50% maximal inhibitory concentrations (IC50s) of HELO on ER and ER cells were 200 and 150 µg/mL after 48 h-treatment. Statistically significant increases in both early and late apoptosis rates were seen in exposed cell lines. ZNF703 expression was less from 4 to 24 h HELO treatment than in untreated cells, and ZNF703 expression was higher in the more invasive MDA-MB-468 cells than in the less invasive MCF-7 cells. Our results demonstrated that HELO induces apoptosis and decreases cell growth in both cell lines. Conclusions: Our data suggest that HELO alters the mRNA levels of ZNF703 gene while inducing apoptotic cell death in breast cancer-derived cell lines. -
A Rare SPRY4 Gene Mutation Is Associated with Anosmia and Adult
CASE REPORT published: 12 November 2019 doi: 10.3389/fendo.2019.00781 ARareSPRY4GeneMutationIs Edited by: Jacques Epelbaum, Associated With Anosmia and Institut National de la Santé et de la Recherche Médicale Adult-Onset Isolated (INSERM), France Reviewed by: Hypogonadotropic Hypogonadism Pei-San Tsai, University of Colorado Boulder, 1,2† 1,3† 1† 1,2† United States Rita Indirli ,BiagioCangiano ,EriseldaProfka ,GiovannaMantovani , 1,3† 1,2† 1,3 † 2 † Stephanie Constantin, Luca Persani ,MauraArosio ,MarcoBonomi * and Emanuele Ferrante * National Institutes of Health (NIH), 1 Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy, 2 Endocrinology Unit, Fondazione United States IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy, 3 Lab of Endocrine and Metabolic Research, Division of *Correspondence: Endocrine and Metabolic Diseases, IRCCS Istituto Auxologico Italiano, Milan, Italy Marco Bonomi [email protected]; [email protected] Background: Isolated hypogonadotropic hypogonadism (IHH) is a rare, clinically Emanuele Ferrante heterogeneous condition, caused by the deficient secretion or action of gonadotropin [email protected] releasing hormone (GnRH). It can manifest with absent or incomplete sexual maturation, † ORCID: or as infertility at adult-age; in a half of cases, IHH is associated with hypo/anosmia Rita Indirli orcid.org/0000-0001-5642-0563 (Kallmann syndrome). Although a growing number of genes are being related to this Biagio Cangiano disease, genetic mutations are currently found only in 40% ofIHHpatients. orcid.org/0000-0002-2658-744X Eriselda Profka Case description: Severe congenital hyposmia was diagnosed in a 25-year-old orcid.org/0000-0002-0001-1530 Caucasian man referred to the Ear-Nose-Throat department ofourclinic.Thepatient Giovanna Mantovani orcid.org/0000-0002-9065-3886 had no cryptorchidism or micropenis and experienced a physiological puberty; past Luca Persani medical history and physical examination were unremarkable. -
Landscape of Somatic Mutations in 560 Breast Cancer Whole-Genome
ARTICLE doi:10.1038/nature17676 Landscape of somatic mutations in 560 breast cancer whole-genome sequences Serena Nik-Zainal1,2, Helen Davies1, Johan Staaf3, Manasa Ramakrishna1, Dominik Glodzik1, Xueqing Zou1, Inigo Martincorena1, Ludmil B. Alexandrov1,4,5, Sancha Martin1, David C. Wedge1, Peter Van Loo1,6, Young Seok Ju1, Marcel Smid7, Arie B. Brinkman8, Sandro Morganella9, Miriam R. Aure10,11, Ole Christian Lingjærde11,12, Anita Langerød10,11, Markus Ringnér3, Sung-Min Ahn13, Sandrine Boyault14, Jane E. Brock15, Annegien Broeks16, Adam Butler1, Christine Desmedt17, Luc Dirix18, Serge Dronov1, Aquila Fatima19, John A. Foekens7, Moritz Gerstung1, Gerrit K. J. Hooijer20, Se Jin Jang21, David R. Jones1, Hyung-Yong Kim22, Tari A. King23, Savitri Krishnamurthy24, Hee Jin Lee21, Jeong-Yeon Lee25, Yilong Li1, Stuart McLaren1, Andrew Menzies1, Ville Mustonen1, Sarah O’Meara1, Iris Pauporté26, Xavier Pivot27, Colin A. Purdie28, Keiran Raine1, Kamna Ramakrishnan1, F. Germán Rodríguez-González7, Gilles Romieu29, Anieta M. Sieuwerts7, Peter T. Simpson30, Rebecca Shepherd1, Lucy Stebbings1, Olafur A. Stefansson31, Jon Teague1, Stefania Tommasi32, Isabelle Treilleux33, Gert G. Van den Eynden18,34, Peter Vermeulen18,34, Anne Vincent-Salomon35, Lucy Yates1, Carlos Caldas36, Laura van’t Veer16, Andrew Tutt37,38, Stian Knappskog39,40, Benita Kiat Tee Tan41,42, Jos Jonkers16, Åke Borg3, Naoto T. Ueno24, Christos Sotiriou17, Alain Viari43,44, P. Andrew Futreal1,45, Peter J. Campbell1, Paul N. Span46, Steven Van Laere18, Sunil R. Lakhani30,47, Jorunn E. Eyfjord31, Alastair M. Thompson28,48, Ewan Birney9, Hendrik G. Stunnenberg8, Marc J. van de Vijver20, John W. M. Martens7, Anne-Lise Børresen-Dale10,11, Andrea L. Richardson15,19, Gu Kong22, Gilles Thomas44 & Michael R. -
The Kinesin Spindle Protein Inhibitor Filanesib Enhances the Activity of Pomalidomide and Dexamethasone in Multiple Myeloma
Plasma Cell Disorders SUPPLEMENTARY APPENDIX The kinesin spindle protein inhibitor filanesib enhances the activity of pomalidomide and dexamethasone in multiple myeloma Susana Hernández-García, 1 Laura San-Segundo, 1 Lorena González-Méndez, 1 Luis A. Corchete, 1 Irena Misiewicz- Krzeminska, 1,2 Montserrat Martín-Sánchez, 1 Ana-Alicia López-Iglesias, 1 Esperanza Macarena Algarín, 1 Pedro Mogollón, 1 Andrea Díaz-Tejedor, 1 Teresa Paíno, 1 Brian Tunquist, 3 María-Victoria Mateos, 1 Norma C Gutiérrez, 1 Elena Díaz- Rodriguez, 1 Mercedes Garayoa 1* and Enrique M Ocio 1* 1Centro Investigación del Cáncer-IBMCC (CSIC-USAL) and Hospital Universitario-IBSAL, Salamanca, Spain; 2National Medicines Insti - tute, Warsaw, Poland and 3Array BioPharma, Boulder, Colorado, USA *MG and EMO contributed equally to this work ©2017 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol. 2017.168666 Received: March 13, 2017. Accepted: August 29, 2017. Pre-published: August 31, 2017. Correspondence: [email protected] MATERIAL AND METHODS Reagents and drugs. Filanesib (F) was provided by Array BioPharma Inc. (Boulder, CO, USA). Thalidomide (T), lenalidomide (L) and pomalidomide (P) were purchased from Selleckchem (Houston, TX, USA), dexamethasone (D) from Sigma-Aldrich (St Louis, MO, USA) and bortezomib from LC Laboratories (Woburn, MA, USA). Generic chemicals were acquired from Sigma Chemical Co., Roche Biochemicals (Mannheim, Germany), Merck & Co., Inc. (Darmstadt, Germany). MM cell lines, patient samples and cultures. Origin, authentication and in vitro growth conditions of human MM cell lines have already been characterized (17, 18). The study of drug activity in the presence of IL-6, IGF-1 or in co-culture with primary bone marrow mesenchymal stromal cells (BMSCs) or the human mesenchymal stromal cell line (hMSC–TERT) was performed as described previously (19, 20). -
SPRY4 Polyclonal Antibody (MAPK) Signaling Pathway
SPRY4 polyclonal antibody (MAPK) signaling pathway. It is positioned upstream of RAS (see HRAS; MIM 190020) activation and impairs Catalog Number: PAB11269 the formation of active GTP-RAS (Leeksma et al., 2002 [PubMed 12027893]).[supplied by OMIM] Regulatory Status: For research use only (RUO) References: Product Description: Rabbit polyclonal antibody raised 1. Genomic structure and promoter characterization of against synthetic peptide of SPRY4. the human Sprouty4 gene, a novel regulator of lung morphogenesis. Ding W, Bellusci S, Shi W, Warburton Immunogen: A synthetic peptide corresponding to D. Am J Physiol Lung Cell Mol Physiol. 2004 amino acids 306-322 of human SPRY4. Jul;287(1):L52-9. Epub 2004 Feb 20. 2. Mammalian Sprouty4 suppresses Ras-independent Host: Rabbit ERK activation by binding to Raf1. Sasaki A, Taketomi T, Kato R, Saeki K, Nonami A, Sasaki M, Kuriyama M, Reactivity: Bovine,Chimpanzee,Dog,Human,Mouse,Rat Saito N, Shibuya M, Yoshimura A. Nat Cell Biol. 2003 Applications: ELISA, IHC-P, WB-Ce May;5(5):427-32. (See our web site product page for detailed applications 3. Human sprouty 4, a new ras antagonist on 5q31, information) interacts with the dual specificity kinase TESK1. Leeksma OC, Van Achterberg TA, Tsumura Y, Toshima Protocols: See our web site at J, Eldering E, Kroes WG, Mellink C, Spaargaren M, http://www.abnova.com/support/protocols.asp or product Mizuno K, Pannekoek H, de Vries CJ. Eur J Biochem. page for detailed protocols 2002 May;269(10):2546-56. Specificity: Expect reactivity only with the SPRY4A splice variant of this protein. Form: Liquid Recommend Usage: ELISA (1:3000-1:12000) Western Blot (1:100-1:1000) Immunohistochemistry (1-10 ug/mL) The optimal working dilution should be determined by the end user.