DOCSLIB.ORG

Epigallocatechin‑3‑Gallate Modulates Long Non‑Coding RNA and Mrna Expression Profiles in Lung Cancer Cells

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Epigallocatechin‑3‑Gallate Modulates Long Non‑Coding RNA and Mrna Expression Profiles in Lung Cancer Cells MOLECULAR MEDICINE REPORTS 19: 1509-1520, 2019 Epigallocatechin‑3‑gallate modulates long non‑coding RNA and mRNA expression profiles in lung cancer cells DONG-LI HU1,2, GUO WANG1,2, JING YU1,2, LI-HUA ZHANG1,2, YUAN-FEI HUANG1,2, DAN WANG1,2 and HONG-HAO ZHOU1,2 1Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, Hunan 410008; 2Hunan Key Laboratory of Pharmacogenetics, Institute of Clinical Pharmacology, Central South University, Changsha, Hunan 410078, P.R. China Received March 12, 2018; Accepted October 26, 2018 DOI: 10.3892/mmr.2019.9816 Abstract. (-)-Epigallocatechin-3-gallate (EGCG), a Introduction major constituent of green tea, is a potential anticancer agent, but the molecular mechanisms of its effects are Lung cancer is one of the most common solid tumors and has not well-understood. The present study was conducted to very high global incidence and mortality rates (1). Although examine the mechanism of EGCG in lung cancer cells. therapeutic treatment of lung cancer has made great progress, Alterations in long non-coding RNAs (lncRNAs) and the prognosis of lung cancer patients remains unsatisfactory and mRNAs were investigated in lung cancer cells treated treatment causes a number of side effects (2). Natural dietary with EGCG by lncRNA microarray analysis. Furthermore, molecules are promising candidates for novel therapeutic agents the functions and signaling pathways regulated by EGCG in cancer. Green tea is one of the most widely consumed bever- were predicted by bioinformatics analysis. A total of ages, worldwide (3). Furthermore, (-)-epigallocatechin-3-gallate 960 lncRNAs and 1,434 mRNAs were significantly (EGCG), the main component of green tea polyphenols, was altered following EGCG treatment. These lncRNAs were demonstrated to have various biological activities and demon- distributed across nearly all human chromosomes and the strates potential as a chemical and therapeutic agent in several mRNAs were involved in the cell cycle and the mitotic cell diseases, including various cancers (3-8) and atherosclerosis (9). cycle process. Through a combination of microarray and Long non-coding RNAs (lncRNAs) are defined as a bioinformatics analysis, 20 mRNAs predicted to serve a key class of transcripts longer than 200 nucleotides (nt) in the role in the EGCG regulation were identified, and certain cytoplasm and nucleus (10-13). LncRNAs, characterized regulatory networks involving EGCG-regulated lncRNAs by the complexity and diversity of their sequences, have were predicted. In conclusion, EGCG affects the expression been implicated in a wide spectrum of cellular activities of various lncRNAs and mRNAs in the cells, therefore and diseases (14,15). Emerging studies have demonstrated affecting cell functions. The results of the present study that certain lncRNAs are frequently abnormally regulated provide an insight into the mechanism of EGCG, which may in several types of cancer and serve important roles in the be useful for therapeutic development. occurrence and development of tumors (16-19). Accumulating evidence has confirmed the activity of EGCG in lung cancer therapy and many lncRNAs and mRNAs are involved in regu- lating tumorigenesis (10,20-22). However, microarray analysis Correspondence to: Dr Guo Wang, Department of Clinical of the differential expression profiles of lncRNAs and mRNAs Pharmacology, Xiangya Hospital, Central South University, in lung cancer cells treated with EGCG has not been reported. 110 Xiangya Road, Changsha, Hunan 410008, P.R. China In the present study, the EGCG-regulated lncRNAs and E-mail: [email protected] mRNAs were investigated in lung cancer cells by bioinfor- matics analysis. Based on the microarray analysis, a set of Abbreviations: EGCG, (-)-epigallocatechin-3-gallate; lncRNAs and mRNAs was identified whose expression levels lncRNAs, long non-coding RNAs; nt, nucleotides; MTT, were significantly modulated by EGCG in lung cancer cells, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; some of which are novel. However, the extent to which these GO, gene ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; FDR, false discovery rate; RT-qPCR, reverse genes are associated with lung cancer cells through EGCG transcription-quantitative polymerase chain reaction; TF, remains unclear and needs to be addressed in the near future. transcription factor Materials and methods Key words: (-)-epigallocatechin-3-gallate, long non-coding RNAs, microarray, lung cancer, bioinformatics analysis Cell culture and cell proliferation assay. The human lung cancer cell lines A549 (lung adenocarcinoma) and NCI-H460 (large cell lung carcinoma) were cultured in Dulbecco's 1510 HU et al: MICROARRAY ANALYSIS OF EGCG IN LUNG CANCER CELLS modified Eagle's medium containing 10% fetal bovine serum (www geneontology.org). The GO database provides a network (Gibco; Thermo Fisher Scientific, Inc., Waltham, MA, USA). of three structured definition terms that describe the properties Cells were plated in 96-well plates (5,000 cells/well) and were of a gene product (25). Pathway analysis of the differentially incubated overnight (37˚C, 5% CO2), followed by treatment expressed genes was performed according to the Kyoto with EGCG (20, 40, 80, 160, 320 µM) and 0 µM EGCG (control Encyclopedia of Genes and Genomes (KEGG) database group) for 24 or 48 h respectively. The MTT-based assay (www.genome.jp/kegg/). Specifically, Fisher's exact test and (Sangon Biotech Co., Ltd., Shanghai, China) was performed to χ2 tests were performed to classify the GO category and select determine viable cell numbers at 37˚C and DMSO was used to the significant pathway. The false discovery rate (FDR) was dissolve the formazan. Absorbance at 570 nm was measured calculated and the threshold of significance was defined as and the 50% maximal inhibitory concentration (IC50) of EGCG P<0.05. FunDO database (http://fundo.nubic.northwestern. for A549 and NCI-H460 cells were calculated by Graphpad edu/) was used for disease analysis. Prism version 6.0 (GraphPad Software, Inc., CA, USA). Network analysis of EGCG target genes. Search Tool for RNA extraction and quality control. Total RNA was extracted Interactions of Chemicals (STITCH; http://stitch.embl. from 1x106 A549 or NCI-H460 cells treated with different de/) is a database of interactions and correlations between concentration of EGCG and control group respectively, compounds and genes. The EGCG direct target genes were using TRIzol reagent (Invitrogen; Thermo Fisher Scientific, searched and analyzed by using STITCH according to the Inc.), purified with a mirVana miRNA Isolation kit (Ambion; reference (26). Search Tool for the Retrieval of Interacting Thermo Fisher Scientific, Inc.) according to the manufac- Genes (STRING, https://string-db.org/) is a database of turer's protocol, and was quantified using a spectrophotometer protein-protein interactions (27). The interaction of EGCG (NanoDrop ND-1000; NanoDrop, Wilmington, DE, USA). direct target gene and differential expression oncogene The RNA integrity of each sample was assessed by capillary affected by EGCG was determined in the STRING database, electrophoresis using the RNA 6000 Nano Lab-on-a-Chip kit and only the interactions with a combined score > 0.4 were and Bioanalyzer 2100 (Agilent Technologies, Santa Clara, CA, considered as significant. Finally, the network of compound USA). Only RNA extracts with RNA integrity values >6 were and gene interactions was mapped. subjected to further analysis. Analysis of lncRNA binding transcription factors. We RNA amplification, labeling, and hybridization. comple- downloaded the transcriptional factors for each of the mentary (c)DNA labeled with a fluorescent dye (Cy5 or 20 differential expression oncogenes most affected by EGCG Cy3-deoxycytidine triphosphate; CapitalBio Technology Co., treatment from the UCSC Genome Browser (http://genome. Ltd., Beijing, China) was produced by Eberwine's linear RNA ucsc.edu/cgi-bin/hgTracks?hgsid=698152999_7PLacukNAM amplification method as previously described (23), and subse- sjS2GSMIFtIxAic9jW). Then, the lncRNA-transcriptional quently RNase H enzymatic reaction (37˚C for 45 min, and factor-oncogene regulatory network was constructed by using followed by 95˚C for 5 min). The labeled cDNAs were purified the LncPro database (http://bioinfo.bjmu.edu.cn/lncpro/) as using a Capital Bioc RNA Amplification and Labeling kit previously described (28). (CapitalBio Corporation, Beijing, China) and then hybridized with specific probes (CapitalBio Technology Co., Ltd.) in a Reverse transcription‑quantitative polymerase chain reaction hybridization oven (Xinghua Analytical Instrument Factory, (RT‑qPCR). The Total RNA of 1x106 A549 cells treated with Jiangsu, China) overnight at 45˚C. 80 µM EGCG for 48 h and the control group cells was extracted as described above respectively. The PrimeScript™ RT Microarray analysis. The expression levels of lncRNAs and Reagent kit (Takara Bio, Inc., Otsu, Japan) was used for cDNA mRNAs were determined using Gene Spring software V13.0 synthesis and genomic DNA removal. qPCR was performed (Agilent Technologies). The differentially expressed lncRNAs using SYBR® Premix Ex Taq™ (Takara Bio, Inc., Otsu, Japan) and mRNAs between the EGCG-treated and control groups and in an ABI 7000 instrument (Applied Biosystems; Thermo were identified based on the threshold values of ≥2 and ≤‑2 Fisher Scientific, Inc.) for 40 cycles (95˚C for 15 sec, 60˚C for fold-change and paired Student's t-test P<0.05.
Load more

Recommended publications
  • Genetic Variants in Humanin Nuclear Isoform Gene Regions Show No Association with Coronary Artery Disease
    Genetic variants in humanin nuclear isoform gene regions show no association with coronary artery disease Mall Eltermaa ( [email protected] ) University of Tartu https://orcid.org/0000-0002-9651-4107 Maili Jakobson University of Tartu Meeme Utt University of Tartu Sulev Kõks Perron Institute for Neurological and Translational Science Reedik Mägi University of Tartu Joel Starkopf Tartu University Hospital Research article Keywords: humanin, humanin-like, coronary artery disease, association study, peptide Posted Date: June 25th, 2019 DOI: https://doi.org/10.21203/rs.2.10582/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Version of Record: A version of this preprint was published at BMC Research Notes on November 21st, 2019. See the published version at https://doi.org/10.1186/s13104-019-4807-x. Loading [MathJax]/jax/output/CommonHTML/jax.js Page 1/7 Abstract Background Coronary artery disease contributes to noncommunicable disease deaths worldwide. In order to make preventive methods more accurate, we need to know more about the development and progress of this pathology, including the genetic aspects. Humanin is a small peptide known for its cytoprotective and anti-apoptotic properties. Our study looked for genomic associations between humanin-like nuclear isoform genes and coronary artery disease using CARDIoGRAMplusC4D Consortium data. Results Lookup from meta-analysis datasets gave single nucleotide polymorphisms in all 13 humanin-like nuclear isoform genes with the lowest P-value for rs6151662 from the MTRNR2L2 gene including the 50 kb anking region in both directions (P-value = 0.0037). Within the gene region alone the top variant was rs78083998 from the MTRNR2L13 region (meta-analysis P-value=0.042).
    [Show full text]
  • A Clinicopathological and Molecular Genetic Analysis of Low-Grade Glioma in Adults
    A CLINICOPATHOLOGICAL AND MOLECULAR GENETIC ANALYSIS OF LOW-GRADE GLIOMA IN ADULTS Presented by ANUSHREE SINGH MSc A thesis submitted in partial fulfilment of the requirements of the University of Wolverhampton for the degree of Doctor of Philosophy Brain Tumour Research Centre Research Institute in Healthcare Sciences Faculty of Science and Engineering University of Wolverhampton November 2014 i DECLARATION This work or any part thereof has not previously been presented in any form to the University or to any other body whether for the purposes of assessment, publication or for any other purpose (unless otherwise indicated). Save for any express acknowledgments, references and/or bibliographies cited in the work, I confirm that the intellectual content of the work is the result of my own efforts and of no other person. The right of Anushree Singh to be identified as author of this work is asserted in accordance with ss.77 and 78 of the Copyright, Designs and Patents Act 1988. At this date copyright is owned by the author. Signature: Anushree Date: 30th November 2014 ii ABSTRACT The aim of the study was to identify molecular markers that can determine progression of low grade glioma. This was done using various approaches such as IDH1 and IDH2 mutation analysis, MGMT methylation analysis, copy number analysis using array comparative genomic hybridisation and identification of differentially expressed miRNAs using miRNA microarray analysis. IDH1 mutation was present at a frequency of 71% in low grade glioma and was identified as an independent marker for improved OS in a multivariate analysis, which confirms the previous findings in low grade glioma studies.
    [Show full text]
  • CSE642 Final Version
    Eindhoven University of Technology MASTER Dimensionality reduction of gene expression data Arts, S. Award date: 2018 Link to publication Disclaimer This document contains a student thesis (bachelor's or master's), as authored by a student at Eindhoven University of Technology. Student theses are made available in the TU/e repository upon obtaining the required degree. The grade received is not published on the document as presented in the repository. The required complexity or quality of research of student theses may vary by program, and the required minimum study period may vary in duration. General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights. • Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain Eindhoven University of Technology MASTER THESIS Dimensionality Reduction of Gene Expression Data Author: S. (Sako) Arts Daily Supervisor: dr. V. (Vlado) Menkovski Graduation Committee: dr. V. (Vlado) Menkovski dr. D.C. (Decebal) Mocanu dr. N. (Nikolay) Yakovets May 16, 2018 v1.0 Abstract The focus of this thesis is dimensionality reduction of gene expression data. I propose and test a framework that deploys linear prediction algorithms resulting in a reduced set of selected genes relevant to a specified case. Abstract In cancer research there is a large need to automate parts of the process of diagnosis, this is mainly to reduce cost, make it faster and more accurate.
    [Show full text]
  • Characterisation of the Genomic Landscape of CRLF2‐Rearranged Acute Lymphoblastic Leukemia
    Characterisation of the Genomic Landscape of CRLF2- rearranged Acute Lymphoblastic Leukemia Lisa J Russell1*, Lisa Jones1, Amir Enshaei1, Stefano Tonin1, Sarra L Ryan1, Jeyanthy Eswaran1 , Sirintra Nakjang2, Elli Papaemmanuil3,4, Jose M C Tubio4, Adele K Fielding5, Ajay Vora6, Peter J Campbell4, Anthony V Moorman1, and Christine J Harrison1 1 Leukaemia Research Cytogenetics Group, Northern Institute for Cancer Research, Newcastle University, Newcastle-upon-Tyne, UK 2 Bioinformatics Support Unit, Newcastle University, Newcastle-upon-Tyne, UK 3 Memorial Sloan Kettering Cancer Center, USA 4 Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, UK 5 Research Department of Haemaoloty, UCL Cancer Institute, London, UK 6 Department of Haematology, Sheffield Children’s Hospital, Sheffield, UK; AVM and CJH contributed equally to this study Running Title – Genomic landscape of CRLF2 rearranged leukemia Correspondence to: Dr Lisa J Russell, Wolfson Childhood Cancer Research Centre, Northern Institute for Cancer Research, Newcastle University, Level 6, Herschel Building, Brewery Lane, Newcastle upon Tyne, NE1 7RU, [email protected]. Acknowledgements Support by: The Kay Kendall Leukaemia Fund, Leuka, European Haematology Association and Bloodwise (formerly Leukaemia and Lymphoma Research) This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process which may lead to differences between this version and the Version of Record. Please cite this article as an ‘Accepted Article’, doi: 10.1002/gcc.22439 This article is protected by copyright. All rights reserved. Genes, Chromosomes & Cancer Page 2 of 147 Deregulated expression of the type I cytokine receptor, CRLF2, is observed in 5-15% of precursor B-cell acute lymphoblastic leukaemia (B-ALL).
    [Show full text]
  • Genetic Variants in Humanin Nuclear Isoform
    Eltermaa et al. BMC Res Notes (2019) 12:759 https://doi.org/10.1186/s13104-019-4807-x BMC Research Notes RESEARCH NOTE Open Access Genetic variants in humanin nuclear isoform gene regions show no association with coronary artery disease Mall Eltermaa1* , Maili Jakobson1, Meeme Utt1,2, Sulev Kõks3,4, Reedik Mägi5 and Joel Starkopf6 Abstract Objective: Coronary artery disease contributes to noncommunicable disease deaths worldwide. In order to make preventive methods more accurate, we need to know more about the development and progress of this pathology, including the genetic aspects. Humanin is a small peptide known for its cytoprotective and anti-apoptotic properties. Our study looked for genomic associations between humanin-like nuclear isoform genes and coronary artery disease using CARDIoGRAMplusC4D Consortium data. Results: Lookup from meta-analysis datasets gave single nucleotide polymorphisms in all 13 humanin-like nuclear isoform genes with the lowest P value for rs6151662 from the MTRNR2L2 gene including the 50 kb fanking region in both directions (P-value 0.0037). Within the gene region alone the top variant was rs78083998 from the MTRNR2L13 region (meta-analysis P-value= 0.042). None of the found associations were statistically signifcant after correction for multiple testing. Lookup for expression= trait loci in these gene regions gave no statistically signifcant variants. Keywords: Humanin, Humanin-like, Coronary artery disease, Association study, Peptide Introduction identifed, expanding the total to 161 [3]. Tere are genes Cardiovascular diseases account for most noncommu- known to have a large efect on, for example, lipoprotein nicable disease (NCD) deaths worldwide [1]. Te WHO metabolism (e.g.
    [Show full text]
  • Characterization of Nucleic Acids from Extracellular Vesicle-Enriched
    Bart et al. BMC Genomics (2021) 22:425 https://doi.org/10.1186/s12864-021-07733-9 RESEARCH Open Access Characterization of nucleic acids from extracellular vesicle-enriched human sweat Geneviève Bart1, Daniel Fischer2, Anatoliy Samoylenko1, Artem Zhyvolozhnyi1, Pavlo Stehantsev1, Ilkka Miinalainen1, Mika Kaakinen1, Tuomas Nurmi1, Prateek Singh1,3, Susanna Kosamo1, Lauri Rannaste4, Sirja Viitala2, Jussi Hiltunen4 and Seppo J Vainio1* Abstract Background: The human sweat is a mixture of secretions from three types of glands: eccrine, apocrine, and sebaceous. Eccrine glands open directly on the skin surface and produce high amounts of water-based fluid in response to heat, emotion, and physical activity, whereas the other glands produce oily fluids and waxy sebum. While most body fluids have been shown to contain nucleic acids, both as ribonucleoprotein complexes and associated with extracellular vesicles (EVs), these have not been investigated in sweat. In this study we aimed to explore and characterize the nucleic acids associated with sweat particles. Results: We used next generation sequencing (NGS) to characterize DNA and RNA in pooled and individual samples of EV-enriched sweat collected from volunteers performing rigorous exercise. In all sequenced samples, we identified DNA originating from all human chromosomes, but only the mitochondrial chromosome was highly represented with 100% coverage. Most of the DNA mapped to unannotated regions of the human genome with some regions highly represented in all samples. Approximately 5 % of the reads were found to map to other genomes: including bacteria (83%), archaea (3%), and virus (13%), identified bacteria species were consistent with those commonly colonizing the human upper body and arm skin.
    [Show full text]
  • Biological Role and Disease Impact of Copy Number Variation in Complex Disease
    University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations 2014 Biological Role and Disease Impact of Copy Number Variation in Complex Disease Joseph Glessner University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Bioinformatics Commons, and the Genetics Commons Recommended Citation Glessner, Joseph, "Biological Role and Disease Impact of Copy Number Variation in Complex Disease" (2014). Publicly Accessible Penn Dissertations. 1286. https://repository.upenn.edu/edissertations/1286 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/1286 For more information, please contact [email protected]. Biological Role and Disease Impact of Copy Number Variation in Complex Disease Abstract In the human genome, DNA variants give rise to a variety of complex phenotypes. Ranging from single base mutations to copy number variations (CNVs), many of these variants are neutral in selection and disease etiology, making difficult the detection of true common orar r e frequency disease-causing mutations. However, allele frequency comparisons in cases, controls, and families may reveal disease associations. Single nucleotide polymorphism (SNP) arrays and exome sequencing are popular assays for genome-wide variant identification. oT limit bias between samples, uniform testing is crucial, including standardized platform versions and sample processing. Bases occupy single points while copy variants occupy segments.
    [Show full text]
  • BRASTIANOS, Kaliopi Priscilla [US/US]; C/O 55 Fruit Street, Boston, Massachusets 021 14 (US)
    ( (51) International Patent Classification: (72) Inventors; and C12Q 1/6886 (2018.01) (71) Applicants: BRASTIANOS, Kaliopi Priscilla [US/US]; c/o 55 Fruit Street, Boston, Massachusets 021 14 (US). (21) International Application Number: ALVAREZ-BRECKENRIDGE, Christopher Allen PCT/US20 19/035252 [US/US]; c/o 55 Fruit Street, Boston, Massachusetts 021 14 (22) International Filing Date: (US). 03 June 2019 (03.06.2019) (72) Inventors: SHALEK, Alexander K.; c/o 77 Massa¬ (25) Filing Language: English chusets Avenue, Cambridge, Massachusetts 02139 (US). CARTER, Scott; c/o 450 Brookline Avenue, Boston, (26) Publication Language: English Massachusetts 02215 (US). PRAKADAN, Sanjay; c/o 77 (30) Priority Data: Massachusetts Avenue, Cambridge, Massachusetts 02139 62/679,728 0 1 June 2018 (01.06.2018) US (US). (71) Applicants: MASSACHUSETTS INSTITUTE OF (74) Agent: SCHER, Michael B. et al.; Johnson, Marcou & TECHNOLOGY [US/US]; 77 Massachusets Avenue, Isaacs, LLC, P.O. Box 691, Hoschton, Georgia 30548 (US). Cambridge, Massachusets 02139 (US). THE GENER¬ (81) Designated States (unless otherwise indicated, for every AL HOSPITAL CORPORATION [US/US]; 55 Fruit kind of national protection av ailable) . AE, AG, AL, AM, Street, Boston, Massachusetts 021 14 (US). DANA-FAR- AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, BZ, BER CANCER INSTITUTE, INC. [US/US]; 450 Brook¬ CA, CH, CL, CN, CO, CR, CU, CZ, DE, DJ, DK, DM, DO, line Avenue, Boston, Massachusetts 02215 (US). DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, (54) Title: METHODS AND COMPOSITIONS FOR DETECTING AND MODULATING MICROENVIRONMENT GENE SIG¬ NATURES FROM THE CSF OF METASTASIS PATIENTS FIG.
    [Show full text]
  • Bioprinted Mcf7 Breast Cancer Cells, an in Vitro Model for Drug Discovery
    University of Texas at El Paso ScholarWorks@UTEP Open Access Theses & Dissertations 2019-01-01 Bioprinted Mcf7 Breast Cancer Cells, An In Vitro Model For Drug Discovery Aleli Campbell University of Texas at El Paso Follow this and additional works at: https://digitalcommons.utep.edu/open_etd Part of the Biomedical Commons Recommended Citation Campbell, Aleli, "Bioprinted Mcf7 Breast Cancer Cells, An In Vitro Model For Drug Discovery" (2019). Open Access Theses & Dissertations. 2834. https://digitalcommons.utep.edu/open_etd/2834 This is brought to you for free and open access by ScholarWorks@UTEP. It has been accepted for inclusion in Open Access Theses & Dissertations by an authorized administrator of ScholarWorks@UTEP. For more information, please contact [email protected]. BIOPRINTED MCF7 BREAST CANCER CELLS, AN IN VITRO MODEL FOR DRUG DISCOVERY ALELI CAMPBELL Doctoral Program in Biomedical Engineering APPROVED Thomas Boland, Ph.D, Chair Armando Varela-Ramirez, Ph.D Wei Qian, Ph.D Alexander Philipovskiy, M.D.,Ph.D Stephen Crites, Ph.D Dean of Graduate School Copyright © by Aleli Campbell 2019 Dedication To my beloved ever patient husband, Ron, and my children, Kevin and Deanna. BIOPRINTED MCF7 BREAST CANCER CELLS, AN IN VITRO MODEL FOR DRUG DISCOVERY by ALELI CAMPBELL, M.S. DISSERTATION Presented to the Faculty of the Graduate School of The University of Texas at El Paso in Partial Fulfillment of the Requirements for the Degree of DOCTOR OF PHILOSOPHY Metallurgical, Materials and Biomedical Engineering THE UNIVERSITY OF TEXAS AT EL PASO December 2019 Acknowledgements I would like to thank my PhD advisor, Dr. Thomas Boland, for his guidance and support during the PhD program.
    [Show full text]
  • SUPPLEMENTARY DATA Supplementary Table 1. Characteristics of the Organ Donors and Human Islet Preparations Used for RNA-Seq
    SUPPLEMENTARY DATA Supplementary Table 1. Characteristics of the organ donors and human islet preparations used for RNA-seq and independent confirmation and mechanistic studies. Gender Age BMI Cause of death Purity (years) (kg/m2) (%) F 77 23.8 Trauma 45 M 36 26.3 CVD 51 M 77 25.2 CVD 62 F 46 22.5 CVD 60 M 40 26.2 Trauma 34 M 59 26.7 NA 58 M 51 26.2 Trauma 54 F 79 29.7 CH 21 M 68 27.5 CH 42 F 76 25.4 CH 30 F 75 29.4 CVD 24 F 73 30.0 CVD 16 M 63 NA NA 46 F 64 23.4 CH 76 M 69 25.1 CH 68 F 23 19.7 Trauma 70 M 47 27.7 CVD 48 F 65 24.6 CH 58 F 87 21.5 Trauma 61 F 72 23.9 CH 62 M 69 25 CVD 85 M 85 25.5 CH 39 M 59 27.7 Trauma 56 F 76 19.5 CH 35 F 50 20.2 CH 70 F 42 23 CVD 48 M 52 24.5 CH 60 F 79 27.5 CH 89 M 56 24.7 Cerebral ischemia 47 M 69 24.2 CVD 57 F 79 28.1 Trauma 61 M 79 23.7 NA 13 M 82 23 CH 61 M 32 NA NA 75 F 23 22.5 Cardiac arrest 46 M 51 NA Trauma 37 Abbreviations: F: Female; M: Male; BMI: Body mass index; CVD: Cardiovascular disease; CH: Cerebral hemorrhage.
    [Show full text]
  • A Molecular Cytogenetic Investigation of Secondary Abnormalities and Clonal Evolution in ETV6-RUNX1 Positive Acute Lymphoblastic Leukaemia
    A molecular cytogenetic investigation of secondary abnormalities and clonal evolution in ETV6-RUNX1 positive acute lymphoblastic leukaemia Halima Hamdan Abdullah Al-Shehhi Thesis submitted for the degree of Doctor of Philosophy Newcastle University Faculty of Medical Sciences Northern Institute for Cancer Research July 2014 Declaration I certify that no part of the material documented in this thesis has previously been submitted for a degree or other qualification in this or any other university. I declare that this thesis represents my own unaided work, carried out by myself, except where it is acknowledged otherwise in the thesis text. Halima Al-Shehhi July 2014 i Acknowledgements I would like to express my sincere gratitude to my supervisors, Professor Anthony Moorman and Professor Christine Harrison for their unstinting support, encouragement, motivation, enthusiasm, and immense knowledge throughout my PhD study and research. Next, I would like to thank the past and present members of the Leukaemia Research Cytogenetic Group: Dr Amy Erhorn, Dr Alem Gabriel, Claire Schwab, Dr Lucy Chilton, Heather Morrison, Dr Lisa Russell, Dr Sarra Ryan, Dino Mašić, Jake Clayton, Alannah Elliott, Stacey Richardson, Dr Amir Enshaie and Dr Paul Sinclair for all support and help in terms of learning new techniques, comprehensive MLPA screening, review scoring of FISH slides, providing cell lines, SNP array analysis, statistical analysis and sharing knowledge/ ideas. Within the wider NICR, I would like to thank Dr Julie Irving, Elizabeth Matheson, Marian Case and the summer placement student: Alysia Davies for their expertise in helping the establishment of copy number q PCR in the lab and providing a positive control cell line.
    [Show full text]
  • Genomic Analysis of Human Spinal Deformity and Characterization of a Zebrafish Disease Model Jillian Gwen Buchan Washington University in St
    Washington University in St. Louis Washington University Open Scholarship All Theses and Dissertations (ETDs) Spring 4-22-2014 Genomic Analysis of Human Spinal Deformity and Characterization of a Zebrafish Disease Model Jillian Gwen Buchan Washington University in St. Louis Follow this and additional works at: https://openscholarship.wustl.edu/etd Recommended Citation Buchan, Jillian Gwen, "Genomic Analysis of Human Spinal Deformity and Characterization of a Zebrafish Disease Model" (2014). All Theses and Dissertations (ETDs). 1223. https://openscholarship.wustl.edu/etd/1223 This Dissertation is brought to you for free and open access by Washington University Open Scholarship. It has been accepted for inclusion in All Theses and Dissertations (ETDs) by an authorized administrator of Washington University Open Scholarship. For more information, please contact [email protected]. WASHINGTON UNIVERSITY IN ST. LOUIS Division of Biology & Biomedical Sciences Molecular Genetics and Genomics Dissertation Examination Committee: Christina A. Gurnett, Chair Carlos Cruchaga Alison M. Goate Matthew I. Goldsmith Kelly R. Monk Lilianna Solnica-Krezel Genomic Analysis of Human Spinal Deformity and Characterization of a Zebrafish Disease Model by Jillian Gwen Buchan A dissertation presented to the Graduate School of Arts and Sciences of Washington University in partial fulfillment of the requirements for the degree of Doctor of Philosophy May 2014 St. Louis, Missouri TABLE OF CONTENTS List of Figures ….………………………………………………………………………… iv List of Tables
    [Show full text]