Differential Regulation of Estrogen Receptor Α Expression in Breast Cancer Cells by Metastasis-Associated Protein 1

Total Page:16

File Type:pdf, Size:1020Kb

Differential Regulation of Estrogen Receptor Α Expression in Breast Cancer Cells by Metastasis-Associated Protein 1 CAN-13-2020R Supplementary Materials Differential Regulation of Estrogen Receptor α Expression in Breast Cancer Cells by Metastasis-Associated Protein 1 Hyun-Jin Kang1, Min-Ho Lee1, Hae-Lim Kang1, Sung-Hae Kim1, Jung-Ranh Ahn1, Hyelin Na1, Tae-Young Na1, Yona Kim2, Je Kyung Seong2, and Mi-Ock Lee1 1College of Pharmacy and Bio-MAX institute, Research Institute of Pharmaceutical Sciences; and 2College of Veterinary Medicine, BK21 Plus Program for Veterinary Science, Seoul National University, Seoul, Korea; Abbreviations ERα, Estrogen receptor alpha; MTA1, Metastasis-associated protein 1; TFAPT2C, Transcription factor AP-2 gamma; IFI16, interferon inducible protein 16; HDAC, Histone deacetylases; shRNA, small hairpin RNA Supplementary Tables Supplementary Table 1. The sequences of RT-PCR, ChIP, siRNA, and shRNA Oligonucleotide Nucleotide sequence Reference RT-PCR sense 5'-ACTGTAGCAGAGTATCTGGTGA-3' NM_001122742 ERα antisense 5'-GGTCTGCAAGGAATGTTCCTA-3' sense 5'-CACGCACATCAGGGGCAA-3' Lee et al., 2012 MTA1 antisense 5'-GTGCGAAGGTGCCCACA-3' sense 5'-CGTGGGCCGCCCTAGGCACCA-3' Yoo et al., 2006 β-actin antisense 5'-TTGGCTTAGGGTTCAGGGGGG-3' ChIP sense 5'-TTAATCTGGGTGGCTGGA-3' ERα promoter (-3849 ~ -3612) I antisense 5'-TACCCTCTCCTGCTGGA-3' sense 5'-AGGAGCTGGCGGAGGGCGTTCG-3' ERα promoter (+1 ~ +127), II antisense 5'-AGCGCATGTCCCGCCGACACGC-3' Macaluso et al., 2007 sense 5'-GCTGTGCTCTTTTTCCAGGT-3' ERα promoter (+146 ~ +377), III antisense 5'-TTGCTGCTGTCCAGGTACAC-3' Woodfield et al., 2009 sense 5'-TGAACCGTCCGCAGCTCAAGATC-3' ERα promoter (+310 ~ +461), IV antisense 5'-GTCTGACCGTAGACCTGCGCGTTG-3' Zhou et al., 2007 sense 5'-GCTGTGCTCTTTTTCCAGGT-3' ERα promoter (+146 ~ +461) ERpro315 antisense 5'-GTCTGACCGTAGACCTGCGCGTTG-3' siRNA sense 5'-GUUCAGCGUGUCCGGCGAGTT-3' Seo et al., 2009 siGFP antisense 5'-CUCGCCGGACACGCUGAACTT-3' sense 5'-AAGACCCUGCUGGCAGAUAAATT-3' Yoo et al., 2006 siMTA1 antisense 5'-UUUAUCUGCCAGCAGGGUCUUTT-3' sense 5'-CCACACUGGAGUCGCCGAAUATT-3' Williams et al., 2009 siTFAP2C antisense 5'-UAGUCGGCGACUGUGUGGTT-3' sense 5'- GCUGGUCCUAACCAAACGUTT-3' Fujiuchi et al., 2004 siIFI16 antisense 5'-ACGUUUGGUUAGGACCAGCTT-3' sense 5'-GCCUCACCGAAUCCGCAUGTT-3' NM_004964.2 siHDAC1 antisense 5'-CAUGCGGAUUCGGUGAGGCTT-3' sense 5'-AAAUUACGGUCCAGGCUAATT-3' NM_006037.3 siHDAC4 antisense 5'-UUAGCCUGGACCGUAAUUUTT-3' sense 5'-GACUGUUAUUAGCACCUUUTT-3' NM_001015053.1 siHDAC5 antisense 5'-AAAGGUGCUAAUAACAGUCTT-3' sense 5'-CCAUUGCCUACGAGUUUAATT-3' NM_006044.2 siHDAC6 antisense 5'-UUAAACUCGUAGGCAAUGGTT-3' shRNA shGFP 5’-GCAAGCTGACCCTGAAGTTCAT-3’ aAddgene (#30323) shMTA1 5’-GCGCATCTTGTTGGACATATT-3’ bTRCN000001336 shTFAP2C 5’-CCTATGTCTGTGAAGCCGAAT-3’ bTRCN0000019747 shIFI16 5’-ACGTTTGAGGTTCCAAATAAA-3’ bTRCN0000369343 aAddgene (http://www.addgene.org/) bTRCN (The shRNA consortium number) Supplementary Table 2. The common target genes of TFAP2C and MTA1. Gene Regulated Regulated by Refseq Description a b Symbol by MTA1 TFAP2C Slc38a1 BF663461 solute carrier family 38, member 10 ↑ ↑ Ociad2 BG291649 OCIA domain containing 2 ↑ ↑ NPR3 NM_000908 natriuretic peptide receptor C/guanylate cyclase C ↑ ↑ Tnfrsf19 AF246998 tumor necrosis factor receptor superfamily, member 19 ↑ ↑ Depdc6 NM_022783 DEP domain containing 6 ↑ ↑ Plcb4 NM_000933 Phospholipase C, beta 4 ↑ ↑ Tspan5 AF065389 tetraspanin 5 ↑ ↑ Tspan15 NM_012339 tetraspanin 15 ↑ ↑ Itga6 NM_000210 integrin, alpha 6 ↓ ↓ Ppap2b AB000889 phosphatidic acid phosphatase type 2B ↓ ↓ Lpin1 AA813260 lipin 1 ↓ ↓ Nagk NM_017567 N-acetylglucosamine kinase ↓ ↓ Trim56 AL512757 tripartite motif-containing 56 ↓ ↓ Nedd9 AW291077 neural precursor cell expressed, developmentally down-regulated ↓ ↓ 9 Svil NM_003174 supervillin ↓ ↓ Sytl2 NM_017695 synaptotagmin-like 2 ↑ ↓ Slc24a3 NM_020689 solute carrier family 24 (sodium/potassium/calcium exchanger), ↑ ↓ member 3 Gpr126 NM_020455 G protein-coupled receptor 126 ↑ ↓ Pqlc3 AL161956 PQ loop repeat containing 3 ↓ ↑ Rgl1 AF186779 ral guanine nucleotide dissociation stimulator-like 1 ↓ ↑ Kal1 AI432167 Kallmann syndrome 1 sequence ↓ ↑ Sulf2 AL034418 sulfatase 2 ↓ ↑ Micall2 AI821474 MICAL-like 2 ↓ ↑ Gprc5b NM_016235 G protein-coupled receptor, family C, group 5, member B ↓ ↑ Stom M81635 stomatin ↓ ↑ Sulf1 AW043713 sulfatase 1 ↓ ↑ a Woodfield et al (2010) b Ghanta et al (2011): 1123 genes varied by 2 ≥ fold, 0.05 ≤ p-value Supplementary Figures Supplementary Figure 1. Epigenetic control of ERpro315 region by MTA1. MCF7 or MDA-MB- 231 cells were transfected with siMTA1 for 48 h. DNA fragments that immunoprecipitated by anti- H3K4me3 and H3K27me3 antibodies were amplified by PCR using primers for ERpro315. Supplementary Fig. 2. Class II HDACs interact with p300 in the presence of TFAP2C. A. Whole cell lysates were immunoprecipitated (IP) with normal IgG, anti-HDAC4, or anti-HDAC5 antibodies, and immunoprecipitates were fractionated and probed by western blotting (WB) using anti-p300, anti- HDAC4 or anti-HDAC5 antibodies. B. MCF7 cells were transfected with siTFAP2C (300 pmol) for 72 h. Whole cell lysates were immunoprecipitated (IP) with normal IgG, anti-HDAC4, or anti- HDAC5 antibodies, and immunoprecipitates were fractionated and probed by western blotting (WB) using anti-p300, anti-HDAC4 or anti-HDAC5 antibodies. Supplementary References Lee MH, Na H, Kim EJ, Lee HW, Lee MO. Poly(ADP-ribosyl)ation of p53 induces gene-specific transcriptional repression of MTA1. Oncogene 2012;31:5099-107. Yoo YG, Kong G, Lee MO. Metastasis-associated protein 1 enhances stability of hypoxia-inducible factor-1alpha protein by recruiting histone deacetylase 1. EMBO J 2006;25:1231-41. Macaluso M, Montanari M, Noto PB, Gregorio V, Bronner C, Giordano A. Epigenetic modulation of estrogen receptor-alpha by pRb family proteins: a novel mechanism in breast cancer. Cancer Res. 2007;67:7731-7. Woodfield GW, Hitchler MJ, Chen Y, Domann FE, Weigel RJ. Interaction of TFAP2C with the estrogen receptor-alpha promoter is controlled by chromatin structure. Clin Cancer Res. 2009;15:3672-9. Zhou Q, Atadja P, Davidson NE. Histone deacetylase inhibitor LBH589 reactivates silenced estrogen receptor alpha (ER) gene expression without loss of DNA hypermethylation. Cancer Biol Ther. 2007;6:64-9. Seo HW, Kim EJ, Na H, Lee MO. Transcriptional activation of hypoxia-inducible factor-1alpha by HDAC4 and HDAC5 involves differential recruitment of p300 and FIH-1. FEBS Lett 2009;583:55-60. Williams CM, Scibetta AG, Friedrich JK, Canosa M, Berlato C, Moss CH, et al. AP-2gamma promotes proliferation in breast tumour cells by direct repression of the CDKN1A gene. EMBO J 2009;28:3591-601. Fujiuchi N, Aglipay JA, Ohtsuka T, Maehara N, Sahin F, Su GH, et al. Requirement of IFI16 for the maximal activation of p53 induced by ionizing radiation. J Biol Chem 2004;279:20339-44. Woodfield GW, Chen Y, Bair TB, Domann FE, Weigel RJ. Identification of primary gene targets of TFAP2C in hormone responsive breast carcinoma cells. Genes Chromosomes Cancer 2010 ;49:948- 62. Ghanta KS, Li DQ, Eswaran J, Kumar R. Gene profiling of MTA1 identifies novel gene targets and functions. PLoS One 2011;6:e17135. Cicatiello L, Mutarelli M, Grober OM, Paris O, Ferraro L, Ravo M et al. Estrogen receptor alpha controls a gene network in luminal-like breast cancer cells comprising multiple transcription factors and microRNAs. Am J Pathol 2010;176:2113-30. .
Recommended publications
  • Activated Peripheral-Blood-Derived Mononuclear Cells
    Transcription factor expression in lipopolysaccharide- activated peripheral-blood-derived mononuclear cells Jared C. Roach*†, Kelly D. Smith*‡, Katie L. Strobe*, Stephanie M. Nissen*, Christian D. Haudenschild§, Daixing Zhou§, Thomas J. Vasicek¶, G. A. Heldʈ, Gustavo A. Stolovitzkyʈ, Leroy E. Hood*†, and Alan Aderem* *Institute for Systems Biology, 1441 North 34th Street, Seattle, WA 98103; ‡Department of Pathology, University of Washington, Seattle, WA 98195; §Illumina, 25861 Industrial Boulevard, Hayward, CA 94545; ¶Medtronic, 710 Medtronic Parkway, Minneapolis, MN 55432; and ʈIBM Computational Biology Center, P.O. Box 218, Yorktown Heights, NY 10598 Contributed by Leroy E. Hood, August 21, 2007 (sent for review January 7, 2007) Transcription factors play a key role in integrating and modulating system. In this model system, we activated peripheral-blood-derived biological information. In this study, we comprehensively measured mononuclear cells, which can be loosely termed ‘‘macrophages,’’ the changing abundances of mRNAs over a time course of activation with lipopolysaccharide (LPS). We focused on the precise mea- of human peripheral-blood-derived mononuclear cells (‘‘macro- surement of mRNA concentrations. There is currently no high- phages’’) with lipopolysaccharide. Global and dynamic analysis of throughput technology that can precisely and sensitively measure all transcription factors in response to a physiological stimulus has yet to mRNAs in a system, although such technologies are likely to be be achieved in a human system, and our efforts significantly available in the near future. To demonstrate the potential utility of advanced this goal. We used multiple global high-throughput tech- such technologies, and to motivate their development and encour- nologies for measuring mRNA levels, including massively parallel age their use, we produced data from a combination of two distinct signature sequencing and GeneChip microarrays.
    [Show full text]
  • To Study Mutant P53 Gain of Function, Various Tumor-Derived P53 Mutants
    Differential effects of mutant TAp63γ on transactivation of p53 and/or p63 responsive genes and their effects on global gene expression. A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science By Shama K Khokhar M.Sc., Bilaspur University, 2004 B.Sc., Bhopal University, 2002 2007 1 COPYRIGHT SHAMA K KHOKHAR 2007 2 WRIGHT STATE UNIVERSITY SCHOOL OF GRADUATE STUDIES Date of Defense: 12-03-07 I HEREBY RECOMMEND THAT THE THESIS PREPARED UNDER MY SUPERVISION BY SHAMA KHAN KHOKHAR ENTITLED Differential effects of mutant TAp63γ on transactivation of p53 and/or p63 responsive genes and their effects on global gene expression BE ACCEPTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF Master of Science Madhavi P. Kadakia, Ph.D. Thesis Director Daniel Organisciak , Ph.D. Department Chair Committee on Final Examination Madhavi P. Kadakia, Ph.D. Steven J. Berberich, Ph.D. Michael Leffak, Ph.D. Joseph F. Thomas, Jr., Ph.D. Dean, School of Graduate Studies 3 Abstract Khokhar, Shama K. M.S., Department of Biochemistry and Molecular Biology, Wright State University, 2007 Differential effect of TAp63γ mutants on transactivation of p53 and/or p63 responsive genes and their effects on global gene expression. p63, a member of the p53 gene family, known to play a role in development, has more recently also been implicated in cancer progression. Mice lacking p63 exhibit severe developmental defects such as limb truncations, abnormal skin, and absence of hair follicles, teeth, and mammary glands. Germline missense mutations of p63 have been shown to be responsible for several human developmental syndromes including SHFM, EEC and ADULT syndromes and are associated with anomalies in the development of organs of epithelial origin.
    [Show full text]
  • Supplemental Materials ZNF281 Enhances Cardiac Reprogramming
    Supplemental Materials ZNF281 enhances cardiac reprogramming by modulating cardiac and inflammatory gene expression Huanyu Zhou, Maria Gabriela Morales, Hisayuki Hashimoto, Matthew E. Dickson, Kunhua Song, Wenduo Ye, Min S. Kim, Hanspeter Niederstrasser, Zhaoning Wang, Beibei Chen, Bruce A. Posner, Rhonda Bassel-Duby and Eric N. Olson Supplemental Table 1; related to Figure 1. Supplemental Table 2; related to Figure 1. Supplemental Table 3; related to the “quantitative mRNA measurement” in Materials and Methods section. Supplemental Table 4; related to the “ChIP-seq, gene ontology and pathway analysis” and “RNA-seq” and gene ontology analysis” in Materials and Methods section. Supplemental Figure S1; related to Figure 1. Supplemental Figure S2; related to Figure 2. Supplemental Figure S3; related to Figure 3. Supplemental Figure S4; related to Figure 4. Supplemental Figure S5; related to Figure 6. Supplemental Table S1. Genes included in human retroviral ORF cDNA library. Gene Gene Gene Gene Gene Gene Gene Gene Symbol Symbol Symbol Symbol Symbol Symbol Symbol Symbol AATF BMP8A CEBPE CTNNB1 ESR2 GDF3 HOXA5 IL17D ADIPOQ BRPF1 CEBPG CUX1 ESRRA GDF6 HOXA6 IL17F ADNP BRPF3 CERS1 CX3CL1 ETS1 GIN1 HOXA7 IL18 AEBP1 BUD31 CERS2 CXCL10 ETS2 GLIS3 HOXB1 IL19 AFF4 C17ORF77 CERS4 CXCL11 ETV3 GMEB1 HOXB13 IL1A AHR C1QTNF4 CFL2 CXCL12 ETV7 GPBP1 HOXB5 IL1B AIMP1 C21ORF66 CHIA CXCL13 FAM3B GPER HOXB6 IL1F3 ALS2CR8 CBFA2T2 CIR1 CXCL14 FAM3D GPI HOXB7 IL1F5 ALX1 CBFA2T3 CITED1 CXCL16 FASLG GREM1 HOXB9 IL1F6 ARGFX CBFB CITED2 CXCL3 FBLN1 GREM2 HOXC4 IL1F7
    [Show full text]
  • HHS Public Access Author Manuscript
    HHS Public Access Author manuscript Author Manuscript Author ManuscriptGenes Dis Author Manuscript. Author manuscript; Author Manuscript available in PMC 2015 March 24. Published in final edited form as: Genes Dis. 2015 March ; 2(1): 46–56. doi:10.1016/j.gendis.2014.10.003. The roles of interferon-inducible p200 family members IFI16 and p204 in innate immune responses, cell differentiation and proliferation Hua Zhaoa,b, Elena Gonzalezgugela, Lei Chengb, Brendon Richbourgha, Lin Nieb,*, and Chuanju Liua,c aDepartment of Orthopaedic Surgery, New York University School of Medicine, New York, NY 10003, United States bDepartment of Spine Surgery, Qilu Hospital of Shandong University, Jinan, 250014, China cDepartment of Cell Biology, New York University School of Medicine, New York, NY 10016, United States Abstract p204 is a member of the interferon-inducible p200 family proteins in mice. The p200 family has been reported to be multifunctional regulators of cell proliferation, differentiation, apoptosis and senescence. Interferon-inducible protein 16 (IFI16) is regarded as the human ortholog of p204 in several studies. This is possibly due to the similarity of their structures. However the consistency of their functions is still elusive. Currently, an emerging focus has been placed upon the role of the p200 proteins as sensors for microbial DNA in innate immune responses and provides new insights into infections as well as autoimmune diseases. This review specially focuses on IFI16 and p204, the member of p200 family in human and murine respectively, and their pathophysiological roles in innate immune responses, cell differentiation and proliferation. Keywords DNA sensor; IFI16; Innate immune; response; Multifunctional; regulator; p204 Introduction p204 is a multifunctional interferon-inducible murine protein in the p200 family (also known as PYHIN or HIN-200 proteins).
    [Show full text]
  • Ten Commandments for a Good Scientist
    Unravelling the mechanism of differential biological responses induced by food-borne xeno- and phyto-estrogenic compounds Ana María Sotoca Covaleda Wageningen 2010 Thesis committee Thesis supervisors Prof. dr. ir. Ivonne M.C.M. Rietjens Professor of Toxicology Wageningen University Prof. dr. Albertinka J. Murk Personal chair at the sub-department of Toxicology Wageningen University Thesis co-supervisor Dr. ir. Jacques J.M. Vervoort Associate professor at the Laboratory of Biochemistry Wageningen University Other members Prof. dr. Michael R. Muller, Wageningen University Prof. dr. ir. Huub F.J. Savelkoul, Wageningen University Prof. dr. Everardus J. van Zoelen, Radboud University Nijmegen Dr. ir. Toine F.H. Bovee, RIKILT, Wageningen This research was conducted under the auspices of the Graduate School VLAG Unravelling the mechanism of differential biological responses induced by food-borne xeno- and phyto-estrogenic compounds Ana María Sotoca Covaleda Thesis submitted in fulfillment of the requirements for the degree of doctor at Wageningen University by the authority of the Rector Magnificus Prof. dr. M.J. Kropff, in the presence of the Thesis Committee appointed by the Academic Board to be defended in public on Tuesday 14 September 2010 at 4 p.m. in the Aula Unravelling the mechanism of differential biological responses induced by food-borne xeno- and phyto-estrogenic compounds. Ana María Sotoca Covaleda Thesis Wageningen University, Wageningen, The Netherlands, 2010, With references, and with summary in Dutch. ISBN: 978-90-8585-707-5 “Caminante no hay camino, se hace camino al andar. Al andar se hace camino, y al volver la vista atrás se ve la senda que nunca se ha de volver a pisar” - Antonio Machado – A mi madre.
    [Show full text]
  • Novel Insights Into the Thaumarchaeota in the Deepest Oceans: Their Metabolism and Potential Adaptation Mechanisms
    Zhong et al. Microbiome (2020) 8:78 https://doi.org/10.1186/s40168-020-00849-2 RESEARCH Open Access Novel insights into the Thaumarchaeota in the deepest oceans: their metabolism and potential adaptation mechanisms Haohui Zhong1,2, Laura Lehtovirta-Morley3, Jiwen Liu1,2, Yanfen Zheng1, Heyu Lin1, Delei Song1, Jonathan D. Todd3, Jiwei Tian4 and Xiao-Hua Zhang1,2,5* Abstract Background: Marine Group I (MGI) Thaumarchaeota, which play key roles in the global biogeochemical cycling of nitrogen and carbon (ammonia oxidizers), thrive in the aphotic deep sea with massive populations. Recent studies have revealed that MGI Thaumarchaeota were present in the deepest part of oceans—the hadal zone (depth > 6000 m, consisting almost entirely of trenches), with the predominant phylotype being distinct from that in the “shallower” deep sea. However, little is known about the metabolism and distribution of these ammonia oxidizers in the hadal water. Results: In this study, metagenomic data were obtained from 0–10,500 m deep seawater samples from the Mariana Trench. The distribution patterns of Thaumarchaeota derived from metagenomics and 16S rRNA gene sequencing were in line with that reported in previous studies: abundance of Thaumarchaeota peaked in bathypelagic zone (depth 1000–4000 m) and the predominant clade shifted in the hadal zone. Several metagenome-assembled thaumarchaeotal genomes were recovered, including a near-complete one representing the dominant hadal phylotype of MGI. Using comparative genomics, we predict that unexpected genes involved in bioenergetics, including two distinct ATP synthase genes (predicted to be coupled with H+ and Na+ respectively), and genes horizontally transferred from other extremophiles, such as those encoding putative di-myo-inositol-phosphate (DIP) synthases, might significantly contribute to the success of this hadal clade under the extreme condition.
    [Show full text]
  • IFI16 and Cgas Cooperate in the Activation of STING During DNA Sensing in Human Keratinocytes
    ARTICLE Received 15 Dec 2015 | Accepted 22 Dec 2016 | Published 13 Feb 2017 DOI: 10.1038/ncomms14392 OPEN IFI16 and cGAS cooperate in the activation of STING during DNA sensing in human keratinocytes Jessica F. Almine1,2,*, Craig A.J. O’Hare1,2,*, Gillian Dunphy1,2, Ismar R. Haga3, Rangeetha J. Naik1, Abdelmadjid Atrih4, Dympna J. Connolly5, Jordan Taylor1, Ian R. Kelsall1, Andrew G. Bowie5, Philippa M. Beard3,6 & Leonie Unterholzner1,2 Many human cells can sense the presence of exogenous DNA during infection though the cytosolic DNA receptor cyclic GMP-AMP synthase (cGAS), which produces the second messenger cyclic GMP-AMP (cGAMP). Other putative DNA receptors have been described, but whether their functions are redundant, tissue-specific or integrated in the cGAS-cGAMP pathway is unclear. Here we show that interferon-g inducible protein 16 (IFI16) cooperates with cGAS during DNA sensing in human keratinocytes, as both cGAS and IFI16 are required for the full activation of an innate immune response to exogenous DNA and DNA viruses. IFI16 is also required for the cGAMP-induced activation of STING, and interacts with STING to promote STING phosphorylation and translocation. We propose that the two DNA sensors IFI16 and cGAS cooperate to prevent the spurious activation of the type I interferon response. 1 Division of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK. 2 Division of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster University, Lancaster LA1 4YQ, UK. 3 The Pirbright Institute, Pirbright, Surrey GU24 0NF, UK. 4 Fingerprints Proteomics Facility, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.
    [Show full text]
  • A Pathologic Link Between Wilms Tumor Suppressor Gene, WT1, And
    Volume 10 Number 1 January 2008 pp. 69–78 69 www.neoplasia.com RESEARCH ARTICLE † Marianne K.-H. Kim*, Jacqueline M. Mason , A Pathologic Link between Wilms ‡ § Chi-Ming Li , Windy Berkofsky-Fessler , ∥ WT1 Le Jiang , Divaker Choubey¶, Paul E. Grundy#, Tumor Suppressor Gene, , ∥ and IFI161,2 Benjamin Tycko and Jonathan D. Licht* *Division of Hematology/Oncology, Feinberg School of Medicine, Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA; †The Campbell Family Institute for Breast Cancer Research at the Ontario, Cancer Institute, Ontario, Canada; ‡Translational Medicine, Amgen, Thousand Oaks, CA, USA; §Section of Bioinformatics, Genetics and Genomics, Hoffmann-La Roche Inc, Nutley, NJ, USA; ∥Institute for Cancer Genetics and Department of Pathology, Columbia University College of Physicians and Surgeons, New York, NY, USA; ¶University of Cincinnati, Cincinnati, OH, USA; #University of Alberta, Alberta, Canada Abstract The Wilms tumor gene (WT1) is mutated or deleted in patients with heredofamilial syndromes associated with the development of Wilms tumors, but is infrequently mutated in sporadic Wilms tumors. By comparing the micro- array profiles of syndromic versus sporadic Wilms tumors and WT1-inducible Saos-2 osteosarcoma cells, we iden- tified interferon-inducible protein 16 (IFI16), a transcriptional modulator, as a differentially expressed gene and a candidate WT1 target gene. WT1 induction in Saos-2 osteosarcoma cells led to strong induction of IFI16 expression and its promoter activity was responsive to the WT1 protein. Immunohistochemical analysis showed that IFI16 and WT1 colocalized in WT1-replete Wilms tumors, but not in normal human midgestation fetal kidneys, suggesting that the ability of WT1 to regulate IFI16 in tumors represented an aberrant pathologic relationship.
    [Show full text]
  • Human Induced Pluripotent Stem Cell–Derived Podocytes Mature Into Vascularized Glomeruli Upon Experimental Transplantation
    BASIC RESEARCH www.jasn.org Human Induced Pluripotent Stem Cell–Derived Podocytes Mature into Vascularized Glomeruli upon Experimental Transplantation † Sazia Sharmin,* Atsuhiro Taguchi,* Yusuke Kaku,* Yasuhiro Yoshimura,* Tomoko Ohmori,* ‡ † ‡ Tetsushi Sakuma, Masashi Mukoyama, Takashi Yamamoto, Hidetake Kurihara,§ and | Ryuichi Nishinakamura* *Department of Kidney Development, Institute of Molecular Embryology and Genetics, and †Department of Nephrology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan; ‡Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan; §Division of Anatomy, Juntendo University School of Medicine, Tokyo, Japan; and |Japan Science and Technology Agency, CREST, Kumamoto, Japan ABSTRACT Glomerular podocytes express proteins, such as nephrin, that constitute the slit diaphragm, thereby contributing to the filtration process in the kidney. Glomerular development has been analyzed mainly in mice, whereas analysis of human kidney development has been minimal because of limited access to embryonic kidneys. We previously reported the induction of three-dimensional primordial glomeruli from human induced pluripotent stem (iPS) cells. Here, using transcription activator–like effector nuclease-mediated homologous recombination, we generated human iPS cell lines that express green fluorescent protein (GFP) in the NPHS1 locus, which encodes nephrin, and we show that GFP expression facilitated accurate visualization of nephrin-positive podocyte formation in
    [Show full text]
  • The Tumor Suppressor HHEX Inhibits Axon Growth When Prematurely Expressed in Developing Central Nervous System Neurons
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by epublications@Marquette Marquette University e-Publications@Marquette Biological Sciences Faculty Research and Biological Sciences, Department of Publications 9-1-2015 The umorT Suppressor HHEX Inhibits Axon Growth when Prematurely Expressed in Developing Central Nervous System Neurons Matthew .T Simpson Marquette University Ishwariya Venkatesh Marquette University Ben L. Callif Marquette University Laura K. Thiel Marquette University Denise M. Coley Marquette University See next page for additional authors Accepted version. Molecular and Cellular Neuroscience, Vol 68 )September 2015): 272-283. DOI. © 2015 Elsevier Inc. Used with permission. NOTICE: this is the author’s version of a work that was accepted for publication in Molecular and Cellular Neuroscience. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Molecular and Cellular Neuroscience, Vol 68 )September 2015): 272-283. DOI. Authors Matthew T. Simpson, Ishwariya Venkatesh, Ben L. Callif, Laura K. Thiel, Denise M. Coley, Kristen N. Winsor, Zimei Wang, Audra A. Kramer, Jessica K. Lerch, and Murray G. Blackmore This article is available at e-Publications@Marquette: https://epublications.marquette.edu/bio_fac/515 NOT THE PUBLISHED VERSION; this is the author’s final, peer-reviewed manuscript. The published version may be accessed by following the link in the citation at the bottom of the page. The Tumor Suppressor HHEX Inhibits Axon Growth When Prematurely Expressed in Developing Central Nervous System Neurons Matthew T.
    [Show full text]
  • Molecular Signatures Differentiate Immune States in Type 1 Diabetes Families
    Page 1 of 65 Diabetes Molecular signatures differentiate immune states in Type 1 diabetes families Yi-Guang Chen1, Susanne M. Cabrera1, Shuang Jia1, Mary L. Kaldunski1, Joanna Kramer1, Sami Cheong2, Rhonda Geoffrey1, Mark F. Roethle1, Jeffrey E. Woodliff3, Carla J. Greenbaum4, Xujing Wang5, and Martin J. Hessner1 1The Max McGee National Research Center for Juvenile Diabetes, Children's Research Institute of Children's Hospital of Wisconsin, and Department of Pediatrics at the Medical College of Wisconsin Milwaukee, WI 53226, USA. 2The Department of Mathematical Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI 53211, USA. 3Flow Cytometry & Cell Separation Facility, Bindley Bioscience Center, Purdue University, West Lafayette, IN 47907, USA. 4Diabetes Research Program, Benaroya Research Institute, Seattle, WA, 98101, USA. 5Systems Biology Center, the National Heart, Lung, and Blood Institute, the National Institutes of Health, Bethesda, MD 20824, USA. Corresponding author: Martin J. Hessner, Ph.D., The Department of Pediatrics, The Medical College of Wisconsin, Milwaukee, WI 53226, USA Tel: 011-1-414-955-4496; Fax: 011-1-414-955-6663; E-mail: [email protected]. Running title: Innate Inflammation in T1D Families Word count: 3999 Number of Tables: 1 Number of Figures: 7 1 For Peer Review Only Diabetes Publish Ahead of Print, published online April 23, 2014 Diabetes Page 2 of 65 ABSTRACT Mechanisms associated with Type 1 diabetes (T1D) development remain incompletely defined. Employing a sensitive array-based bioassay where patient plasma is used to induce transcriptional responses in healthy leukocytes, we previously reported disease-specific, partially IL-1 dependent, signatures associated with pre and recent onset (RO) T1D relative to unrelated healthy controls (uHC).
    [Show full text]
  • Target Gene Gene Description Validation Diana Miranda
    Supplemental Table S1. Mmu-miR-183-5p in silico predicted targets. TARGET GENE GENE DESCRIPTION VALIDATION DIANA MIRANDA MIRBRIDGE PICTAR PITA RNA22 TARGETSCAN TOTAL_HIT AP3M1 adaptor-related protein complex 3, mu 1 subunit V V V V V V V 7 BTG1 B-cell translocation gene 1, anti-proliferative V V V V V V V 7 CLCN3 chloride channel, voltage-sensitive 3 V V V V V V V 7 CTDSPL CTD (carboxy-terminal domain, RNA polymerase II, polypeptide A) small phosphatase-like V V V V V V V 7 DUSP10 dual specificity phosphatase 10 V V V V V V V 7 MAP3K4 mitogen-activated protein kinase kinase kinase 4 V V V V V V V 7 PDCD4 programmed cell death 4 (neoplastic transformation inhibitor) V V V V V V V 7 PPP2R5C protein phosphatase 2, regulatory subunit B', gamma V V V V V V V 7 PTPN4 protein tyrosine phosphatase, non-receptor type 4 (megakaryocyte) V V V V V V V 7 EZR ezrin V V V V V V 6 FOXO1 forkhead box O1 V V V V V V 6 ANKRD13C ankyrin repeat domain 13C V V V V V V 6 ARHGAP6 Rho GTPase activating protein 6 V V V V V V 6 BACH2 BTB and CNC homology 1, basic leucine zipper transcription factor 2 V V V V V V 6 BNIP3L BCL2/adenovirus E1B 19kDa interacting protein 3-like V V V V V V 6 BRMS1L breast cancer metastasis-suppressor 1-like V V V V V V 6 CDK5R1 cyclin-dependent kinase 5, regulatory subunit 1 (p35) V V V V V V 6 CTDSP1 CTD (carboxy-terminal domain, RNA polymerase II, polypeptide A) small phosphatase 1 V V V V V V 6 DCX doublecortin V V V V V V 6 ENAH enabled homolog (Drosophila) V V V V V V 6 EPHA4 EPH receptor A4 V V V V V V 6 FOXP1 forkhead box P1 V
    [Show full text]