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A Key Genomic Signature Associated with Lymphovascular Invasion in Head and Neck Squamous Cell Carcinoma
A key genomic signature associated with lymphovascular invasion in head and neck squamous cell carcinoma Jian Zhang Aliated Cancer hospital & Institute of Guangzhou Medical University Huali Jiang Aliated Donghua Hospital of Sun Yat-sen University Tao Xie Aliated Cancer Hospital of Guangzhou Medical University Baiyao Wang Aliated Cancer Hospital of Guangzhou Medical Unversity Xiaoting Huang Aliated Cancer Hospital & Institute of Guangzhou Medical University Jie Lin Aliated Cancer Hospital & Institute of Guangzhou Medical University Anan Xu Aliated Cancer Hospital of Guangzhou Medical University Rong Li Aliated Cancer Hospital & Institute of Guangzhou Medical University Yawei Yuan ( [email protected] ) Guangzhou Medical University Aliated Cancer Hospital Research article Keywords: lymphovascular invasion, head and neck squamous cell carcinoma, hub genes, TCGA, weighted gene co-expression network analysis Posted Date: January 16th, 2020 DOI: https://doi.org/10.21203/rs.2.18349/v2 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/24 Abstract Objective: Lymphovascular invasion (LOI), a key pathological feature of head and neck squamous cell carcinoma (HNSCC), predicts poor survival. However, the associated clinical characteristics remain uncertain, and the molecular mechanisms are largely unknown. Methods: Weighted gene co-expression network analysis was performed to construct gene co-expression networks and investigate the relationship between modules and LOI clinical trait. Functional enrichment and KEGG pathway enrichment analysis were performed for differentially expressed genes using DAVID database. The protein-protein interaction network was constructed using Cytoscape software, and module analysis was performed using MCODE. Prognosis role and expression analysis was further validated by survival analysis, GEPIA analysis and HPA database. -
Supplementary Table 1: Adhesion Genes Data Set
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like, -
Apoptotic Genes As Potential Markers of Metastatic Phenotype in Human Osteosarcoma Cell Lines
17-31 10/12/07 14:53 Page 17 INTERNATIONAL JOURNAL OF ONCOLOGY 32: 17-31, 2008 17 Apoptotic genes as potential markers of metastatic phenotype in human osteosarcoma cell lines CINZIA ZUCCHINI1, ANNA ROCCHI2, MARIA CRISTINA MANARA2, PAOLA DE SANCTIS1, CRISTINA CAPANNI3, MICHELE BIANCHINI1, PAOLO CARINCI1, KATIA SCOTLANDI2 and LUISA VALVASSORI1 1Dipartimento di Istologia, Embriologia e Biologia Applicata, Università di Bologna, Via Belmeloro 8, 40126 Bologna; 2Laboratorio di Ricerca Oncologica, Istituti Ortopedici Rizzoli; 3IGM-CNR, Unit of Bologna, c/o Istituti Ortopedici Rizzoli, Via di Barbiano 1/10, 40136 Bologna, Italy Received May 29, 2007; Accepted July 19, 2007 Abstract. Metastasis is the most frequent cause of death among malignant primitive bone tumor, usually developing in children patients with osteosarcoma. We have previously demonstrated and adolescents, with a high tendency to metastasize (2). in independent experiments that the forced expression of Metastases in osteosarcoma patients spread through peripheral L/B/K ALP and CD99 in U-2 OS osteosarcoma cell lines blood very early and colonize primarily the lung, and later markedly reduces the metastatic ability of these cancer cells. other skeleton districts (3). Since disseminated hidden micro- This behavior makes these cell lines a useful model to assess metastases are present in 80-90% of OS patients at the time the intersection of multiple and independent gene expression of diagnosis, the identification of markers of invasiveness signatures concerning the biological problem of dissemination. and metastasis forms a target of paramount importance in With the aim to characterize a common transcriptional profile planning the treatment of osteosarcoma lesions and enhancing reflecting the essential features of metastatic behavior, we the prognosis. -
Profiling Microdissected Epithelium and Stroma to Model Genomic Signatures for Cervical Carcinogenesis Accommodating for Covariates
Research Article Profiling Microdissected Epithelium and Stroma to Model Genomic Signatures for Cervical Carcinogenesis Accommodating for Covariates David Gius,1 Margo C. Funk,2 Eric Y. Chuang,1 Sheng Feng,3 Phyllis C. Huettner,4 Loan Nguyen,2 C. Matthew Bradbury,1 Mark Mishra,1 Shuping Gao,1 Barbara M. Buttin,2 David E. Cohn,2 Matthew A. Powell,2 Neil S. Horowitz,2 Bradford P. Whitcomb,2 and JanetS. Rader 2 1Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland and 2Division of Gynecologic Oncology, Department of Obstetrics and Gynecology; 3Division of Biostatistics; and 4Lauren V. Ackerman Laboratory of Surgical Pathology, Washington University School of Medicine, St. Louis, Missouri Abstract (CIN 1–3) and finally to squamous cell carcinoma antigen (SCCA) This study is the first comprehensive, integrated approach to have been well characterized. Histologically, CIN 1 consists of examine grade-specific changes in gene expression along the immature basal-type cells involving the lower third of the entire neoplastic spectrum of cervical intraepithelial neoplasia epithelium. In CIN 2, these immature basal-type cells involve more (CIN) in the process of cervical carcinogenesis. This was than the lower third, whereas CIN 3 involves the full thickness of the accomplished by identifying gene expression signatures of epithelium. In addition, higher CIN grades exhibit nuclear crowding, disease progression using cDNA microarrays to analyze RNA pleomorphism, loss of cell polarity, and increased mitotic activity from laser-captured microdissected epithelium and underlying (1). These transitions seemto be well conserved and, as such, stroma from normal cervix, graded CINs, cancer, and patient- provide an intriguing systemto use genomicsto identify the early matched normal cervical tissues. -
A Dissertation Entitled the Androgen Receptor
A Dissertation entitled The Androgen Receptor as a Transcriptional Co-activator: Implications in the Growth and Progression of Prostate Cancer By Mesfin Gonit Submitted to the Graduate Faculty as partial fulfillment of the requirements for the PhD Degree in Biomedical science Dr. Manohar Ratnam, Committee Chair Dr. Lirim Shemshedini, Committee Member Dr. Robert Trumbly, Committee Member Dr. Edwin Sanchez, Committee Member Dr. Beata Lecka -Czernik, Committee Member Dr. Patricia R. Komuniecki, Dean College of Graduate Studies The University of Toledo August 2011 Copyright 2011, Mesfin Gonit This document is copyrighted material. Under copyright law, no parts of this document may be reproduced without the expressed permission of the author. An Abstract of The Androgen Receptor as a Transcriptional Co-activator: Implications in the Growth and Progression of Prostate Cancer By Mesfin Gonit As partial fulfillment of the requirements for the PhD Degree in Biomedical science The University of Toledo August 2011 Prostate cancer depends on the androgen receptor (AR) for growth and survival even in the absence of androgen. In the classical models of gene activation by AR, ligand activated AR signals through binding to the androgen response elements (AREs) in the target gene promoter/enhancer. In the present study the role of AREs in the androgen- independent transcriptional signaling was investigated using LP50 cells, derived from parental LNCaP cells through extended passage in vitro. LP50 cells reflected the signature gene overexpression profile of advanced clinical prostate tumors. The growth of LP50 cells was profoundly dependent on nuclear localized AR but was independent of androgen. Nevertheless, in these cells AR was unable to bind to AREs in the absence of androgen. -
Plasma Cells in Vitro Generation of Long-Lived Human
Downloaded from http://www.jimmunol.org/ by guest on September 24, 2021 is online at: average * The Journal of Immunology , 32 of which you can access for free at: 2012; 189:5773-5785; Prepublished online 16 from submission to initial decision 4 weeks from acceptance to publication November 2012; doi: 10.4049/jimmunol.1103720 http://www.jimmunol.org/content/189/12/5773 In Vitro Generation of Long-lived Human Plasma Cells Mario Cocco, Sophie Stephenson, Matthew A. Care, Darren Newton, Nicholas A. Barnes, Adam Davison, Andy Rawstron, David R. Westhead, Gina M. Doody and Reuben M. Tooze J Immunol cites 65 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription http://www.jimmunol.org/content/suppl/2012/11/16/jimmunol.110372 0.DC1 This article http://www.jimmunol.org/content/189/12/5773.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2012 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 24, 2021. The Journal of Immunology In Vitro Generation of Long-lived Human Plasma Cells Mario Cocco,*,1 Sophie Stephenson,*,1 Matthew A. -
KIF23 Enhances Cell Proliferation in Pancreatic Ductal Adenocarcinoma and Is a Potent Therapeutic Target
1394 Original Article Page 1 of 15 KIF23 enhances cell proliferation in pancreatic ductal adenocarcinoma and is a potent therapeutic target Chun-Tao Gao1#, Jin Ren2#, Jie Yu1,3#, Sheng-Nan Li1, Xiao-Fan Guo1, Yi-Zhang Zhou1 1Department of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin’s Clinical Research Center for Cancer, Tianjin, China; 2Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Taiyuan, China; 3The First Hospital of Shanxi Medical University, Taiyuan, China Contributions: (I) Conception and design: CT Gao, J Ren; (II) Administrative support: CT Gao; (III) Provision of study materials or patients: J Yu; (IV) Collection and assembly of data: J Ren, SN Li, YZ Zhou; (V) Data analysis and interpretation: XF Guo, J Ren; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. #These authors contributed equally to this work. Correspondence to: Chun-Tao Gao. Department of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin’s Clinical Research Center for Cancer, Huan-hu-xi Road, He-xi District, Tianjin 300060, China. Email: [email protected]. Background: In recent research, high expression of kinesin family member 23 (KIF23), one of the kinesin motor proteins involved in the regulation of cytokinesis, has been shown to be related to poor prognosis in glioma and paclitaxel-resistant gastric cancer, as a results of the enhancement of proliferation, migration, and invasion. In this study, we analyzed the role of KIF23 in the progression of pancreatic ductal adenocarcinoma. -
Highlights of Glycosylation and Adhesion
Highlights of glycosylation and adhesion related genes involved in myogenesis Vincent Grassot, Anne da Silva, James Saliba, Abderrahman Maftah, Fabrice Dupuy, Jean-Michel Petit To cite this version: Vincent Grassot, Anne da Silva, James Saliba, Abderrahman Maftah, Fabrice Dupuy, et al.. Highlights of glycosylation and adhesion related genes involved in myogenesis. BMC Genomics, BioMed Central, 2014, 15 (1), pp.3-17. 10.1186/1471-2164-15-621. hal-01211986 HAL Id: hal-01211986 https://hal.archives-ouvertes.fr/hal-01211986 Submitted on 27 May 2020 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Grassot et al. BMC Genomics 2014, 15:621 http://www.biomedcentral.com/1471-2164/15/621 RESEARCH ARTICLE Open Access Highlights of glycosylation and adhesion related genes involved in myogenesis Vincent Grassot, Anne Da Silva, James Saliba, Abderrahman Maftah, Fabrice Dupuy and Jean-Michel Petit* Abstract Background: Myogenesis is initiated by myoblast differentiation and fusion to form myotubes and muscle fibres. A population of myoblasts, known as satellite cells, is responsible for post-natal growth of muscle and for its regeneration. This differentiation requires many changes in cell behaviour and its surrounding environment. -
Cell Adhesion Molecules in Normal Skin and Melanoma
biomolecules Review Cell Adhesion Molecules in Normal Skin and Melanoma Cian D’Arcy and Christina Kiel * Systems Biology Ireland & UCD Charles Institute of Dermatology, School of Medicine, University College Dublin, D04 V1W8 Dublin, Ireland; [email protected] * Correspondence: [email protected]; Tel.: +353-1-716-6344 Abstract: Cell adhesion molecules (CAMs) of the cadherin, integrin, immunoglobulin, and selectin protein families are indispensable for the formation and maintenance of multicellular tissues, espe- cially epithelia. In the epidermis, they are involved in cell–cell contacts and in cellular interactions with the extracellular matrix (ECM), thereby contributing to the structural integrity and barrier for- mation of the skin. Bulk and single cell RNA sequencing data show that >170 CAMs are expressed in the healthy human skin, with high expression levels in melanocytes, keratinocytes, endothelial, and smooth muscle cells. Alterations in expression levels of CAMs are involved in melanoma propagation, interaction with the microenvironment, and metastasis. Recent mechanistic analyses together with protein and gene expression data provide a better picture of the role of CAMs in the context of skin physiology and melanoma. Here, we review progress in the field and discuss molecular mechanisms in light of gene expression profiles, including recent single cell RNA expression information. We highlight key adhesion molecules in melanoma, which can guide the identification of pathways and Citation: D’Arcy, C.; Kiel, C. Cell strategies for novel anti-melanoma therapies. Adhesion Molecules in Normal Skin and Melanoma. Biomolecules 2021, 11, Keywords: cadherins; GTEx consortium; Human Protein Atlas; integrins; melanocytes; single cell 1213. https://doi.org/10.3390/ RNA sequencing; selectins; tumour microenvironment biom11081213 Academic Editor: Sang-Han Lee 1. -
Integrin Alpha 11 in the Regulation of the Myofibroblast Phenotype: Implications for Fibrotic Diseases
Integrin alpha 11 in the regulation of the myofibroblast phenotype: implications for fibrotic diseases The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Bansal, R., S. Nakagawa, S. Yazdani, J. van Baarlen, A. Venkatesh, A. P. Koh, W. Song, et al. 2017. “Integrin alpha 11 in the regulation of the myofibroblast phenotype: implications for fibrotic diseases.” Experimental & Molecular Medicine 49 (11): e396. doi:10.1038/ emm.2017.213. http://dx.doi.org/10.1038/emm.2017.213. Published Version doi:10.1038/emm.2017.213 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:34651853 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA OPEN Experimental & Molecular Medicine (2017) 49, e396; doi:10.1038/emm.2017.213 Official journal of the Korean Society for Biochemistry and Molecular Biology www.nature.com/emm ORIGINAL ARTICLE Integrin alpha 11 in the regulation of the myofibroblast phenotype: implications for fibrotic diseases Ruchi Bansal1, Shigeki Nakagawa2,3, Saleh Yazdani1, Joop van Baarlen4, Anu Venkatesh2,3, Anna P Koh2,3, Won-Min Song2,3, Nicolas Goossens2,3, Hideo Watanabe5, Mary B Beasley3,6, Charles A Powell7, Gert Storm1,8, Naftali Kaminski9, Harry van Goor10, Scott L Friedman2,3, Yujin Hoshida2,3 and Jai Prakash1,11,12 Tissue fibrosis, characterized by excessive accumulation of aberrant extracellular matrix (ECM) produced by myofibroblasts, is a growing cause of mortality worldwide. -
How Does SUMO Participate in Spindle Organization?
cells Review How Does SUMO Participate in Spindle Organization? Ariane Abrieu * and Dimitris Liakopoulos * CRBM, CNRS UMR5237, Université de Montpellier, 1919 route de Mende, 34090 Montpellier, France * Correspondence: [email protected] (A.A.); [email protected] (D.L.) Received: 5 July 2019; Accepted: 30 July 2019; Published: 31 July 2019 Abstract: The ubiquitin-like protein SUMO is a regulator involved in most cellular mechanisms. Recent studies have discovered new modes of function for this protein. Of particular interest is the ability of SUMO to organize proteins in larger assemblies, as well as the role of SUMO-dependent ubiquitylation in their disassembly. These mechanisms have been largely described in the context of DNA repair, transcriptional regulation, or signaling, while much less is known on how SUMO facilitates organization of microtubule-dependent processes during mitosis. Remarkably however, SUMO has been known for a long time to modify kinetochore proteins, while more recently, extensive proteomic screens have identified a large number of microtubule- and spindle-associated proteins that are SUMOylated. The aim of this review is to focus on the possible role of SUMOylation in organization of the spindle and kinetochore complexes. We summarize mitotic and microtubule/spindle-associated proteins that have been identified as SUMO conjugates and present examples regarding their regulation by SUMO. Moreover, we discuss the possible contribution of SUMOylation in organization of larger protein assemblies on the spindle, as well as the role of SUMO-targeted ubiquitylation in control of kinetochore assembly and function. Finally, we propose future directions regarding the study of SUMOylation in regulation of spindle organization and examine the potential of SUMO and SUMO-mediated degradation as target for antimitotic-based therapies. -
Genomics and Functional Genomics of Malignant Pleural Mesothelioma
International Journal of Molecular Sciences Review Genomics and Functional Genomics of Malignant Pleural Mesothelioma Ece Cakiroglu 1,2 and Serif Senturk 1,2,* 1 Izmir Biomedicine and Genome Center, Izmir 35340, Turkey; [email protected] 2 Department of Genome Sciences and Molecular Biotechnology, Izmir International Biomedicine and Genome Institute, Dokuz Eylul University, Izmir 35340, Turkey * Correspondence: [email protected] Received: 22 July 2020; Accepted: 20 August 2020; Published: 1 September 2020 Abstract: Malignant pleural mesothelioma (MPM) is a rare, aggressive cancer of the mesothelial cells lining the pleural surface of the chest wall and lung. The etiology of MPM is strongly associated with prior exposure to asbestos fibers, and the median survival rate of the diagnosed patients is approximately one year. Despite the latest advancements in surgical techniques and systemic therapies, currently available treatment modalities of MPM fail to provide long-term survival. The increasing incidence of MPM highlights the need for finding effective treatments. Targeted therapies offer personalized treatments in many cancers. However, targeted therapy in MPM is not recommended by clinical guidelines mainly because of poor target definition. A better understanding of the molecular and cellular mechanisms and the predictors of poor clinical outcomes of MPM is required to identify novel targets and develop precise and effective treatments. Recent advances in the genomics and functional genomics fields have provided groundbreaking insights into the genomic and molecular profiles of MPM and enabled the functional characterization of the genetic alterations. This review provides a comprehensive overview of the relevant literature and highlights the potential of state-of-the-art genomics and functional genomics research to facilitate the development of novel diagnostics and therapeutic modalities in MPM.