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SATB1 in Malignant T Cells.
Fredholm, Simon; Willerslev-Olsen, Andreas; Met, Özcan; Kubat, Linda; Gluud, Maria; Mathiasen, Sarah L; Friese, Christina; Blümel, Edda; Petersen, David L; Hu, Tengpeng; Nastasi, Claudia; Lindahl, Lise M; Buus, Terkild B; Krejsgaard, Thorbjørn; Wasik, Mariusz A; Kopp, Katharina L; Koralov, Sergei B; Persson, Jenny L; Bonefeld, Charlotte M; Geisler, Carsten; Woetmann, Anders; Iversen, Lars; Becker, Jürgen C; Ødum, Niels.
Afiliación
  • Fredholm S; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Willerslev-Olsen A; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Met Ö; Center for Cancer Immune Therapy, Department of Hematology, Herlev Hospital, University of Copenhagen, Herlev, Denmark; Department of Oncology, Herlev Hospital, University of Copenhagen, Herlev, Denmark.
  • Kubat L; Translational Skin Cancer Research, German Cancer Consortium (DKTK and DKFZ), Partner Site Essen, Essen, Germany.
  • Gluud M; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Mathiasen SL; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Friese C; Center for Cancer Immune Therapy, Department of Hematology, Herlev Hospital, University of Copenhagen, Herlev, Denmark.
  • Blümel E; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Petersen DL; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Hu T; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Nastasi C; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Lindahl LM; Department of Dermatology, Aarhus University Hospital, Skejby, Aarhus, Denmark.
  • Buus TB; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Krejsgaard T; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Wasik MA; Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
  • Kopp KL; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Koralov SB; Department of Pathology, New York University School of Medicine, New York, New York, USA.
  • Persson JL; Division of Experimental Cancer Research, Department of Translational Medicine, Lund University, Clinical Research Centre, Malmö, Sweden; Division of Basal Tumor Biology, Department of Molecular Biology, Umeå University, Umeå, Sweden.
  • Bonefeld CM; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Geisler C; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Woetmann A; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
  • Iversen L; Department of Dermatology, Aarhus University Hospital, Skejby, Aarhus, Denmark.
  • Becker JC; Translational Skin Cancer Research, German Cancer Consortium (DKTK and DKFZ), Partner Site Essen, Essen, Germany. Electronic address: j.becker@dkfz-heidelberg.de.
  • Ødum N; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark. Electronic address: ndum@sund.ku.dk.
J Invest Dermatol ; 138(8): 1805-1815, 2018 08.
Article en En | MEDLINE | ID: mdl-29751003
Deficient expression of SATB1 hampers thymocyte development and results in inept T-cell lineages. Recent data implicate dysregulated SATB1 expression in the pathogenesis of mycosis fungoides, the most frequent variant of cutaneous T-cell lymphoma. Here, we report on a disease stage-associated decrease of SATB1 expression and an inverse expression of STAT5 and SATB1 in situ. STAT5 inhibited SATB1 expression through induction of microRNA-155. Decreased SATB1 expression triggered enhanced expression of IL-5 and IL-9 (but not IL-6 and IL-32), whereas increased SATB1 expression had the opposite effect, indicating that the microRNA-155 target SATB1 is a repressor of IL-5 and IL-9 in malignant T cells. In accordance, inhibition of STAT5 and its upstream activator JAK3 triggered increased SATB1 expression and a concomitant suppression of IL-5 and IL-9 expression in malignant T cells. In conclusion, we provide a mechanistic link between the proto-oncogenic JAK3/STAT5/microRNA-155 pathway, SATB1, and cytokines linked to CTCL severity and progression, indicating that SATB1 dysregulation is involved in cutaneous T-cell lymphoma pathogenesis.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Cutáneas / Linfocitos T / Micosis Fungoide / Proteínas de Unión a la Región de Fijación a la Matriz / MicroARNs Tipo de estudio: Etiology_studies / Incidence_studies / Observational_studies / Risk_factors_studies Límite: Humans Idioma: En Revista: J Invest Dermatol Año: 2018 Tipo del documento: Article País de afiliación: Dinamarca Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Cutáneas / Linfocitos T / Micosis Fungoide / Proteínas de Unión a la Región de Fijación a la Matriz / MicroARNs Tipo de estudio: Etiology_studies / Incidence_studies / Observational_studies / Risk_factors_studies Límite: Humans Idioma: En Revista: J Invest Dermatol Año: 2018 Tipo del documento: Article País de afiliación: Dinamarca Pais de publicación: Estados Unidos