S100A14 Rabbit Pab

Leader in Biomolecular Solutions for Life Science S100A14 Rabbit pAb Catalog No.: A10394 1 Publications Basic Information Background Catalog No. This gene encodes a member of the S100 protein family which contains an EF-hand A10394 motif and binds calcium. The gene is located in a cluster of S100 genes on chromosome 1. Levels of the encoded protein have been found to be lower in cancerous tissue and Observed MW associated with metastasis suggesting a tumor suppressor function (PMID: 19956863, 11kDa 19351828). Calculated MW 11kDa Category Primary antibody Applications WB, IHC, IF Cross-Reactivity Human, Mouse, Rat Recommended Dilutions Immunogen Information WB 1:500 - 1:2000 Gene ID Swiss Prot 57402 Q9HCY8 IHC 1:50 - 1:200 Immunogen 1:50 - 1:200 IF Recombinant fusion protein containing a sequence corresponding to amino acids 1-104 of human S100A14 (NP_065723.1). Synonyms S100A14;BCMP84;S100A15 Contact Product Information www.abclonal.com Source Isotype Purification Rabbit IgG Affinity purification Storage Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3. Validation Data Western blot analysis of extracts of various cell lines, using S100A14 antibody (A10394) at 1:1000 dilution. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (AS014) at 1:10000 dilution. Lysates/proteins: 25ug per lane. Blocking buffer: 3% nonfat dry milk in TBST. Detection: ECL Basic Kit (RM00020). Exposure time: 30s. Immunohistochemistry of paraffin- Immunofluorescence analysis of C6 cells Immunofluorescence analysis of HeLa cells embedded human esophageal using using S100A14 Rabbit pAb (A10394) at using S100A14 Rabbit pAb (A10394) at S100A14 Rabbit pAb (A10394) at dilution of dilution of 1:100 (40x lens). Blue: DAPI for dilution of 1:100 (40x lens). Blue: DAPI for 1:100 (40x lens). nuclear staining. nuclear staining. Immunofluorescence analysis of NIH-3T3 cells using S100A14 Rabbit pAb (A10394) at dilution of 1:100 (40x lens). Blue: DAPI for nuclear staining. Antibody | Protein | ELISA Kits | Enzyme | NGS | Service For research use only. Not for therapeutic or diagnostic purposes. Please visit http://abclonal.com for a complete listing of recommended products..

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PARSANA-DISSERTATION-2020.Pdf
DECIPHERING TRANSCRIPTIONAL PATTERNS OF GENE REGULATION: A COMPUTATIONAL APPROACH by Princy Parsana A dissertation submitted to The Johns Hopkins University in conformity with the requirements for the degree of Doctor of Philosophy Baltimore, Maryland July, 2020 © 2020 Princy Parsana All rights reserved Abstract With rapid advancements in sequencing technology, we now have the ability to sequence the entire human genome, and to quantify expression of tens of thousands of genes from hundreds of individuals. This provides an extraordinary opportunity to learn phenotype relevant genomic patterns that can improve our understanding of molecular and cellular processes underlying a trait. The high dimensional nature of genomic data presents a range of computational and statistical challenges. This dissertation presents a compilation of projects that were driven by the motivation to efficiently capture gene regulatory patterns in the human transcriptome, while addressing statistical and computational challenges that accompany this data. We attempt to address two major difficulties in this domain: a) artifacts and noise in transcriptomic data, andb) limited statistical power. First, we present our work on investigating the effect of artifactual variation in gene expression data and its impact on trans-eQTL discovery. Here we performed an in-depth analysis of diverse pre-recorded covariates and latent confounders to understand their contribution to heterogeneity in gene expression measurements. Next, we discovered 673 trans-eQTLs across 16 human tissues using v6 data from the Genotype Tissue Expression (GTEx) project. Finally, we characterized two trait-associated trans-eQTLs; one in Skeletal Muscle and another in Thyroid. Second, we present a principal component based residualization method to correct gene expression measurements prior to reconstruction of co-expression networks.
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Identification of Mechanisms and Pathways Involved in MLL2-Mediated Tumorigenesis by Chun-Chi Chang Department of Pathology Duke University Date:_______________________ Approved: ___________________________ Yiping He, Supervisor ___________________________ Salvatore Pizzo ___________________________ Hai Yan Thesis submitted in partial fulfillment of the requirements for the degree of Master of Science in the Department of Pathology in the Graduate School of Duke University 2013 ABSTRACT Identification of Mechanisms and Pathways Involved in MLL2-Mediated Tumorigenesis by Chun-Chi Chang Department of Pathology Duke University Date:_______________________ Approved: ___________________________ Yiping He, Supervisor ___________________________ Salvatore Pizzo ___________________________ Hai Yan An abstract of a thesis submitted in partial fulfillment of the requirements for the degree of Master of Science in the Department of Pathology in the Graduate School of Duke University 2013 Copyright by Chun-Chi Chang 2013 Abstract Myeloid/lymphoid or mixed-lineage leukemia (MLL)-family genes encode histone lysine methyltransferases that play important roles in epigenetic regulation of gene transcription, and these genes are frequently mutated in human cancers. While MLL1 and MLL4 have been the most extensively studied, MLL2 and its homolog MLL3 are not well-understood. Specifically, little is known regarding the extent of global MLL2 involvement in the regulation of gene expression and the mechanism underlying its alterations in mediating tumorigenesis. To study the role of MLL2 in tumorigenesis, we somatically knocked out MLL2 in a colorectal carcinoma cell line, HCT116. We observed that the MLL2 loss of function results in significant reduction of cell growth and multinuclear morphology. We further profiled MLL2 regulated genes and pathways by analyzing gene expression in MLL2 wild-type versus MLL2-null isogenic cell lines.
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UNIVERSITY of CALIFORNIA, IRVINE Gene Regulatory
UNIVERSITY OF CALIFORNIA, IRVINE Gene Regulatory Mechanisms in Epithelial Specification and Function DISSERTATION submitted in partial satisfaction of the requirements for the degree of DOCTOR OF PHILOSOPHY in Biomedical Sciences by Rachel Herndon Klein Dissertation Committee: Professor Bogi Andersen, M.D., Chair Professor Xing Dai, Ph.D. Professor Anand Ganesan, M.D. Professor Ali Mortazavi, Ph.D Professor Kyoko Yokomori, Ph.D 2015 © 2015 Rachel Herndon Klein DEDICATION To My parents, my sisters, my husband, and my friends for your love and support, and to Ben with all my love. ii TABLE OF CONTENTS Page LIST OF FIGURES iv LIST OF TABLES vi ACKNOWLEDGMENTS vii CURRICULUM VITAE viii-ix ABSTRACT OF THE DISSERTATION x-xi CHAPTER 1: INTRODUCTION 1 CHAPTER 2: Cofactors of LIM domain (CLIM) proteins regulate corneal epithelial progenitor cell function through noncoding RNA H19 22 CHAPTER 3: KLF7 regulates the corneal epithelial progenitor cell state acting antagonistically to KLF4 49 CHAPTER 4: GRHL3 interacts with super enhancers and the neuronal repressor REST to regulate keratinocyte differentiation and migration 77 CHAPTER 5: Methods 103 CHAPTER 6: Summary and Conclusions 111 REFERENCES 115 iii LIST OF FIGURES Page Figure 1-1. Structure and organization of the epidermis. 3 Figure 1-2. Structure of the limbus, and cornea epithelium. 4 Figure 1-3. Comparison of H3K4 methylating SET enzymes between S. cerevisiae, D. melanogaster, and H. sapiens. 18 Figure 1-4. The WRAD complex associates with Trithorax SET enzymes. 18 Figure 1-5. Model for GRHL3, PcG, and TrX –mediated regulation of epidermal differentiation genes. 19 Figure 2-1. Microarray gene expression analysis of postnatal day 3 (P3) whole mouse corneas reveals genes and pathways with altered expression in K14-DN-Clim mice.
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Bioinformatics Mining of the Dark Matter Proteome For
BIOINFORMATICS MINING OF THE DARK MATTER PROTEOME FOR CANCER TARGETS DISCOVERY by Ana Paula Delgado A Thesis Submitted to the Faculty of The Charles E. Schmidt College of Science In Partial Fulfillment of the Requirements for the Degree of Master of Science Florida Atlantic University Boca Raton, Florida May 2015 Copyright 2015 by Ana Paula Delgado ii ACKNOWLEDGEMENTS I would first like to thank Dr. Narayanan for his continuous encouragement, guidance, and support during the past two years of my graduate education. It has truly been an unforgettable experience working in his laboratory. I also want to express gratitude to my external advisor Professor Van de Ven from the University of Leuven, Belgium for his constant involvement and assistance on my project. Moreover, I would like to thank Dr. Binninger and Dr. Dawson-Scully for their advice and for agreeing to serve on my thesis committee. I also thank provost Dr. Perry for his involvement in my project. I thank Jeanine Narayanan for editorial assistance with the publications and with this dissertation. It has been a pleasure working with various undergraduate students some of whom became lab mates including Pamela Brandao, Maria Julia Chapado and Sheilin Hamid. I thank them for their expert help in the projects we were involved in. Lastly, I want to express my profound thanks to my parents and brother for their unconditional love, support and guidance over the last couple of years. They were my rock when I was in doubt and never let me give up. I would also like to thank my boyfriend Spencer Daniel and best friends for being part of an incredible support system.
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A Grainyhead-Like 2/Ovo-Like 2 Pathway Regulates Renal Epithelial Barrier Function and Lumen Expansion
BASIC RESEARCH www.jasn.org A Grainyhead-Like 2/Ovo-Like 2 Pathway Regulates Renal Epithelial Barrier Function and Lumen Expansion † ‡ | Annekatrin Aue,* Christian Hinze,* Katharina Walentin,* Janett Ruffert,* Yesim Yurtdas,*§ | Max Werth,* Wei Chen,* Anja Rabien,§ Ergin Kilic,¶ Jörg-Dieter Schulzke,** †‡ Michael Schumann,** and Kai M. Schmidt-Ott* *Max Delbrueck Center for Molecular Medicine, Berlin, Germany; †Experimental and Clinical Research Center, and Departments of ‡Nephrology, §Urology, ¶Pathology, and **Gastroenterology, Charité Medical University, Berlin, Germany; and |Berlin Institute of Urologic Research, Berlin, Germany ABSTRACT Grainyhead transcription factors control epithelial barriers, tissue morphogenesis, and differentiation, but their role in the kidney is poorly understood. Here, we report that nephric duct, ureteric bud, and collecting duct epithelia express high levels of grainyhead-like homolog 2 (Grhl2) and that nephric duct lumen expansion is defective in Grhl2-deficient mice. In collecting duct epithelial cells, Grhl2 inactivation impaired epithelial barrier formation and inhibited lumen expansion. Molecular analyses showed that GRHL2 acts as a transcrip- tional activator and strongly associates with histone H3 lysine 4 trimethylation. Integrating genome-wide GRHL2 binding as well as H3 lysine 4 trimethylation chromatin immunoprecipitation sequencing and gene expression data allowed us to derive a high-confidence GRHL2 target set. GRHL2 transactivated a group of genes including Ovol2, encoding the ovo-like 2 zinc finger transcription factor, as well as E-cadherin, claudin 4 (Cldn4), and the small GTPase Rab25. Ovol2 induction alone was sufficient to bypass the requirement of Grhl2 for E-cadherin, Cldn4,andRab25 expression. Re-expression of either Ovol2 or a combination of Cldn4 and Rab25 was sufficient to rescue lumen expansion and barrier formation in Grhl2-deficient collecting duct cells.
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Expression of S100 Protein Family Members in the Pathogenesis of Bladder Tumors
ANTICANCER RESEARCH 27: 3051-3058 (2007) Expression of S100 Protein Family Members in the Pathogenesis of Bladder Tumors RUISHENG YAO1, ANTONIO LOPEZ-BELTRAN2, GREGORY T. MACLENNAN3, RODOLFO MONTIRONI4, JOHN N. EBLE5 and LIANG CHENG5,6 1Department of Surgery and The Alvin J. Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO, U.S.A.; 2Department of Pathology, Cordoba University, Cordoba, Spain; 3Department of Pathology, Case Western Reserve University, Cleveland, Ohio, U.S.A.; 4Institute of Pathological Anatomy and Histopathology, School of Medicine, Polytechnic University of the Marche Region (Ancona), United Hospitals, Ancona, Italy; Departments of 5Pathology and Laboratory Medicine, and 6Urology, Indiana University School of Medicine, Indianapolis, IN, U.S.A. Abstract. The S100 proteins act as multifactional signaling expressions in bladder cancers. Our results indicate that factors that are involved in the regulation of diverse cellular differential expression of S100 gene family members is processes. To explore the involvement of S100 genes in bladder characteristic of bladder cancers and these genes may play cancers, S100 gene expressions were systematically evaluated important roles in bladder tumorigenesis and progression. at the RNA level by microarray and real-time PCR. Total RNAs were obtained from 4-hydroxybutyl(butyl)nitrosamine Bladder cancer is the sixth most common malignancy in (OH-BBN)-induced mouse and rat bladder cancers, human developed countries. It ranks as the fourth and ninth most bladder cancers and matched normal bladder urothelium. common cancer in men and women in the United States, Microarray analysis was performed on mouse and rat bladder respectively. It is estimated that about 61,420 cases will be cancers; real-time PCR was performed in mouse, rat and newly diagnosed in the USA and 13,060 patients were human bladder cancers and their matched normal urothelium expected to die from disseminated disease in 2006 (1).
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393LN V 393P 344SQ V 393P Probe Set Entrez Gene
393LN v 393P 344SQ v 393P Entrez fold fold probe set Gene Gene Symbol Gene cluster Gene Title p-value change p-value change chemokine (C-C motif) ligand 21b /// chemokine (C-C motif) ligand 21a /// chemokine (C-C motif) ligand 21c 1419426_s_at 18829 /// Ccl21b /// Ccl2 1 - up 393 LN only (leucine) 0.0047 9.199837 0.45212 6.847887 nuclear factor of activated T-cells, cytoplasmic, calcineurin- 1447085_s_at 18018 Nfatc1 1 - up 393 LN only dependent 1 0.009048 12.065 0.13718 4.81 RIKEN cDNA 1453647_at 78668 9530059J11Rik1 - up 393 LN only 9530059J11 gene 0.002208 5.482897 0.27642 3.45171 transient receptor potential cation channel, subfamily 1457164_at 277328 Trpa1 1 - up 393 LN only A, member 1 0.000111 9.180344 0.01771 3.048114 regulating synaptic membrane 1422809_at 116838 Rims2 1 - up 393 LN only exocytosis 2 0.001891 8.560424 0.13159 2.980501 glial cell line derived neurotrophic factor family receptor alpha 1433716_x_at 14586 Gfra2 1 - up 393 LN only 2 0.006868 30.88736 0.01066 2.811211 1446936_at --- --- 1 - up 393 LN only --- 0.007695 6.373955 0.11733 2.480287 zinc finger protein 1438742_at 320683 Zfp629 1 - up 393 LN only 629 0.002644 5.231855 0.38124 2.377016 phospholipase A2, 1426019_at 18786 Plaa 1 - up 393 LN only activating protein 0.008657 6.2364 0.12336 2.262117 1445314_at 14009 Etv1 1 - up 393 LN only ets variant gene 1 0.007224 3.643646 0.36434 2.01989 ciliary rootlet coiled- 1427338_at 230872 Crocc 1 - up 393 LN only coil, rootletin 0.002482 7.783242 0.49977 1.794171 expressed sequence 1436585_at 99463 BB182297 1 - up 393
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Original Article Comparative Membrane Proteomic Analysis Between Lung Adenocarcinoma and Normal Tissue by Itraq Labeling Mass Spectrometry
Am J Transl Res 2014;6(3):267-280 www.ajtr.org /ISSN:1943-8141/AJTR0000125 Original Article Comparative membrane proteomic analysis between lung adenocarcinoma and normal tissue by iTRAQ labeling mass spectrometry Xuede Zhang, Wei Li, Yanli Hou, Zequn Niu, Yujie Zhong, Yuping Zhang, Shuanying Yang Department of Respiratory Medicine, The Second Affiliated Hospital of Medical College, Xi’an Jiaotong University, Xi’an, Shannxi 710004, China Received February 28, 2014; Accepted April 10, 2014; Epub May 15, 2014; Published May 30, 2014 Abstract: Lung adenocarcinoma, the most common type of lung cancer, has increased in recent years. Prognosis is still poor, and pathogenesis remains unclear. This study aimed to investigate the membrane protein profile dif- ferences between lung adenocarcinoma and normal tissue. Manual microdissection was used to isolate the tar- get cells from tumor tissue and normal tissue. iTRAQ labeling combined with 2D-LC-MS/MS yielded a differential expression profile of membrane proteins. Bioinformatic analysis was performed using Gene Ontology, WEGO, PID, and KEGG. S100A14 protein was selectively verified by Western blotting. The relationship of S100A14 expression with clinicopathological features in lung cancer patients was evaluated using immunohistochemistry. As a result, 568 differential proteins were identified; 257 proteins were upregulated and 311 were downregulated. Of these proteins, 48% were found to be membrane bound or membrane associated. These proteins enable the physiologi- cal functions of binding, catalysis, molecular transduction, transport, and molecular structure. For these differential proteins, 35 pathways were significantly enriched through the Pathway Interaction Database, whereas 19 pathways were enriched via KEGG. The overexpression and cellular distribution of S100A14 in lung cancer were confirmed.
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Differentially Expressed Genes in Aneurysm Tissue Compared With
On-line Table: Differentially expressed genes in aneurysm tissue compared with those in control tissue Fold False Discovery Direction of Gene Entrez Gene Name Function Change P Value Rate (q Value) Expression AADAC Arylacetamide deacetylase Positive regulation of triglyceride 4.46 1.33E-05 2.60E-04 Up-regulated catabolic process ABCA6 ATP-binding cassette, subfamily A (ABC1), Integral component of membrane 3.79 9.15E-14 8.88E-12 Up-regulated member 6 ABCC3 ATP-binding cassette, subfamily C (CFTR/MRP), ATPase activity, coupled to 6.63 1.21E-10 7.33E-09 Up-regulated member 3 transmembrane movement of substances ABI3 ABI family, member 3 Peptidyl-tyrosine phosphorylation 6.47 2.47E-05 4.56E-04 Up-regulated ACKR1 Atypical chemokine receptor 1 (Duffy blood G-protein–coupled receptor signaling 3.80 7.95E-10 4.18E-08 Up-regulated group) pathway ACKR2 Atypical chemokine receptor 2 G-protein–coupled receptor signaling 0.42 3.29E-04 4.41E-03 Down-regulated pathway ACSM1 Acyl-CoA synthetase medium-chain family Energy derivation by oxidation of 9.87 1.70E-08 6.52E-07 Up-regulated member 1 organic compounds ACTC1 Actin, ␣, cardiac muscle 1 Negative regulation of apoptotic 0.30 7.96E-06 1.65E-04 Down-regulated process ACTG2 Actin, ␥2, smooth muscle, enteric Blood microparticle 0.29 1.61E-16 2.36E-14 Down-regulated ADAM33 ADAM domain 33 Integral component of membrane 0.23 9.74E-09 3.95E-07 Down-regulated ADAM8 ADAM domain 8 Positive regulation of tumor necrosis 4.69 2.93E-04 4.01E-03 Up-regulated factor (ligand) superfamily member 11 production ADAMTS18
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Targets of the Tumor Suppressor Mir-200 in Regulation of the Epithelial–Mesenchymal Transition in Cancer
Published OnlineFirst October 10, 2011; DOI: 10.1158/0008-5472.CAN-11-0964 Cancer Tumor and Stem Cell Biology Research Targets of the Tumor Suppressor miR-200 in Regulation of the Epithelial–Mesenchymal Transition in Cancer Mark J. Schliekelman1 , Don L. Gibbons2,3, Vitor M. Faca1, Chad J. Creighton4, Zain H. Rizvi2, Qing Zhang1, Chee-Hong Wong1, Hong Wang1, Christin Ungewiss2, Young-Ho Ahn2, Dong-Hoon Shin2, Jonathan M. Kurie2, and Samir M. Hanash1 Abstract The microRNA-200 (miR-200) family restricts epithelial–mesenchymal transition (EMT) and metastasis in tumor cell lines derived from mice that develop metastatic lung adenocarcinoma. To determine the mechanisms responsible for EMT and metastasis regulated by this microRNA, we conducted a global liquid chromatography/ tandem mass spectrometry analysis to compare metastatic and nonmetastatic murine lung adenocarcinoma cells which had undergone EMT because of loss of miR-200. An analysis of syngeneic tumors generated by these cells identified multiple novel proteins linked to metastasis. In particular, the analysis of conditioned media, cell surface proteins, and whole-cell lysates from metastatic and nonmetastatic cells revealed large-scale modifica- tions in the tumor microenvironment. Specific increases were documented in extracellular matrix (ECM) proteins, peptidases, and changes in distribution of cell adhesion proteins in the metastatic cell lines. Integrating proteomic data from three subproteomes, we defined constituents of a multilayer protein network that both regulated and mediated the effects of TGFb. Lastly, we identified ECM proteins and peptidases that were directly regulated by miR-200. Taken together, our results reveal how expression of miR-200 alters the tumor microenvironment to inhibit the processes of EMT and metastasis.
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Inline-Supplementary-Material-6.Pdf
Table S3. Transcriptome analysis page 1 Table S3. Transcriptomic analysis of cultured mutant and wildtype skin fibroblast. Gene Protein name GeneCards annotation OMIM Locus Fold FDR PATIENTS CONTROLS - change (n=2) (n=4) ment apoptosis apoptosis Keratinocyte Keratinocyte inflammation differentiation Neurodevelop cell growth and growth cell FPKM [SD] FPKM [SD] genes up-regulated in patient cells ESRP1 epithelial ESRP1 is an mRNA splicing factor that regulates the *612959, the gene product is an 8:95653301 - present - 0.011 0.3547 0.0038 0.0000 0.0000 splicing formation of epithelial cell-specific isoforms. epithelial cell-type-specific splicing 95719694 absent regulatory Specifically regulates the expression of FGFR2-IIIb, regulator. Mutations in ESRP1 are protein 1 an epithelial cell-specific isoform of FGFR2. Also potentially associated with autosomal regulates the splicing of CD44, CTNND1, ENAH, recessive deafness type 109. three transcripts that undergo changes in splicing during the epithelial-to-mesenchymal transition (EMT). CERS3 ceramide CERS3 is a member of the ceramide synthase family #615023, autosomal recessive 15:100913143 - present - 0.011 0.1844 0.0118 0.0000 0.0000 synthase 3 of genes. The ceramide synthase enzymes regulate congenital ichthyosis type 9, 101085200 absent sphingolipid synthesis by catalyzing the formation characterized by collodian membrane at of ceramides from sphingoid base and acyl-CoA birth, acanthosis, orthohyperkeratosis, substrates. This family member is involved in the fine erythrodermic scales, palmoplantar synthesis of ceramides with ultra-long-chain acyl- hyperlinearity. moieties (ULC-Cers), important to the epidermis in its role in creating a protective barrier from the environment. GJB6 gap junction GJB6 encodes one of the connexin proteins.
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Identification of Potential Gene and Microrna Biomarkers for Colon Cancer by an Integrated Bioinformatical Approach
29 Original Article Identification of potential gene and microRNA biomarkers for colon cancer by an integrated bioinformatical approach Qingxia Ma1*, Jingyi Song2*, Zhen Chen2, Lei Li2, Bin Wang2, Ningning He2 1Department of Pharmacology, School of Pharmacy, 2School of Basic Medical Sciences, Qingdao University, Qingdao 266021, China Contributions: (I) Conception and design: N He, B Wang; (II) Administrative support: B Wang; (III) Provision of study materials or patients: Q Ma, J Song, Z Chen; (IV) Collection and assembly of data: Q Ma, J Song, L Li; (V) Data analysis and interpretation: N He, B Wang; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. *These authors contributed equally to this work. Correspondence to: Bin Wang. School of Basic Medical Sciences, Qingdao University, 38 Dengzhou Road, Qingdao, 266021, China. Email: [email protected]; Ningning He. School of Basic Medical Sciences, Qingdao University, 38 Dengzhou Road, Qingdao, 266021, China. Email: [email protected]. Background: A unique resource for genomic studies is the NCI-60 cancer cell line panel, which provides various publicly available datasets, including gene and microRNA (miRNA) transcripts, whole-exome sequencing, DNA copy number, and protein levels against 59 cancer cell lines. In this study, we aimed to identify differentially expressed genes (DEGs) and differentially expressed miRNAs (DEMs) for colon cancers by analyzing NCI-60 gene and miRNA expression profiles. Methods: The real-time quantitative RT-PCR (qRT-PCR) was used to validate the identified candidate genes and miRNAs. The functional enrichment analysis and pathway analysis were performed for DEGs and the network analysis was performed for predicted miRNA targets of DEMs.
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