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  • 1.
    Fugazza, Cristina
    et al.
    Università di Milano-Bicocca, Italy.
    Barbarani, Gloria
    Università di Milano-Bicocca, Italy.
    Elangovan, Sudharshan
    Università di Milano-Bicocca, Italy.
    Marini, Maria Giuseppina
    Istituto di Ricerca Genetica e Biomedica del Consiglio Nazionale delle Ricerche, Italy.
    Giolitto, Serena
    Università di Milano-Bicocca, Italy.
    Font-Monclus, Isaura
    Università di Milano-Bicocca, Italy.
    Marongiu, Maria Franca
    Istituto di Ricerca Genetica e Biomedica del Consiglio Nazionale delle Ricerche, Italy.
    Manunza, Laura
    Universita degli Studi di Cagliari, Italy.
    Strouboulis, John
    King's College London, United Kingdom.
    Cantù, Claudio
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Gasparri, Fabio
    Nerviano Medical Sciences S.r.l., Nerviano, Italy.
    Barabino, Silvia M. L.
    Università di Milano-Bicocca, Milano, Italy.
    Nakamura, Yukio
    RIKEN BioResource Research Center, Japan.
    Ottolenghi, Sergio
    Università di Milano-Bicocca, Milano, Italy.
    Moi, Paolo
    Universita degli Studi di Cagliari, Italy.
    Ronchi, Antonella Ellena
    Università di Milano-Bicocca, Milano, Italy.
    The Coup-TFII orphan nuclear receptor is an activator of the γ-globin gene2020In: Haematologica, ISSN 0390-6078, E-ISSN 1592-8721Article in journal (Refereed)
    Abstract [en]

    The human fetal γ-globin gene is repressed in the adult stage through complex regulatory mechanisms involving transcription factors and epigenetic modifiers. Reversing γ-globin repression, or maintaining its expression by manipulating regulatory mechanisms, has become a major clinical goal in the treatment of β-hemoglobinopathies. Here, we identify the orphan nuclear receptor Coup-TFII (NR2F2/ARP-1) as an embryonic/fetal stage activator of γ-globin expression. We show that Coup-TFII is expressed in early erythropoiesis of yolk sac origin, together with embryonic/fetal globins. When overexpressed in adult cells (including peripheral blood cells from human healthy donors and β039 thalassemic patients) Coup-TFII activates the embryonic/fetal globins genes, overcoming the repression imposed by the adult erythroid environment. Conversely, the knock-out of Coup-TFII increases the β/γ+β globin ratio. Molecular analysis indicates that Coup-TFII binds in vivo to the β-locus and contributes to its conformation. Overall, our data identify Coup-TFII as a specific activator of the γ-globin gene.

  • 2.
    Pagella, Pierfrancesco
    et al.
    Orofacial Development & Regeneration, Institute of Oral Biology, University of Zurich, Zurich, Switzerland.
    Cantù, Claudio
    Orofacial Development & Regeneration, Institute of Oral Biology, University of Zurich, Zurich, Switzerland.
    Mitsiadis, Thimios A.
    Orofacial Development & Regeneration, Institute of Oral Biology, University of Zurich, Zurich, Switzerland.
    Linking dental pathologies and cancer via Wnt signalling2017In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 8, no 59, p. 99213-99214Article in journal (Refereed)
  • 3.
    Varum, Sandra
    et al.
    University of Zurich, Switzerland.
    Baggiolini, Arianna
    University of Zurich, Switzerland.
    Zurkirchen, Luis
    University of Zurich, Switzerland.
    Atak, Zeynep Kalender
    Laboratory of Computational Biology, Belgium; Department of Human Genetics, Belgium.
    Cantù, Claudio
    University of Zurich, Switzerland.
    Marzorati, Elisa
    University of Zurich, Switzerland.
    Bossart, Raphaël
    University of Zurich, Switzerland.
    Wouters, Jasper
    Laboratory of Computational Biology, Leuven, Belgium; KU Leuven, Leuven, Belgium.
    Häusel, Jessica
    University of Zurich, Switzerland.
    Tuncer, Eylül
    University of Zurich, Switzerland.
    Zingg, Daniel
    University of Zurich, Switzerland.
    Veen, Dominiek
    University of Zurich, Switzerland.
    John, Nessy
    University of Zurich, Switzerland.
    Balz, Marcel
    University of Zurich, Switzerland.
    Levesque, Mitchell P
    University of Zurich, Switzerland.
    Basler, Konrad
    University of Zurich, Switzerland.
    Aerts, Stein
    University of Zurich, Switzerland.
    Zamboni, Nicola
    University of Zurich, Switzerland.
    Dummer, Reinhard
    University of Zurich, Switzerland.
    Sommer, Lukas
    University of Zurich, Switzerland.
    Yin Yang 1 Orchestrates a Metabolic Program Required for Both Neural Crest Development and Melanoma Formation2019In: Cell Stem Cell, ISSN 1934-5909, E-ISSN 1875-9777, Vol. 24, no 4, p. 637-653.e9Article in journal (Refereed)
    Abstract [en]

    Increasing evidence suggests that cancer cells highjack developmental programs for disease initiation and progression. Melanoma arises from melanocytes that originate during development from neural crest stem cells (NCSCs). Here, we identified the transcription factor Yin Yang 1 (Yy1) as an NCSCs regulator. Conditional deletion of Yy1 in NCSCs resulted in stage-dependent hypoplasia of all major neural crest derivatives due to decreased proliferation and increased cell death. Moreover, conditional ablation of one Yy1 allele in a melanoma mouse model prevented tumorigenesis, indicating a particular susceptibility of melanoma cells to reduced Yy1 levels. Combined RNA sequencing (RNA-seq), chromatin immunoprecipitation (ChIP)-seq, and untargeted metabolomics demonstrated that YY1 governs multiple metabolic pathways and protein synthesis in both NCSCs and melanoma. In addition to directly regulating a metabolic gene set, YY1 can act upstream of MITF/c-MYC as part of a gene regulatory network controlling metabolism. Thus, both NCSC development and melanoma formation depend on an intricate YY1-controlled metabolic program.

  • 4.
    Zimmerli, Dario
    et al.
    Univ Zurich, Switzerland.
    Cecconi, Virginia
    Univ Zurich, Switzerland.
    Valenta, Tomas
    Univ Zurich, Switzerland.
    Hausmann, George
    Univ Zurich, Switzerland.
    Cantù, Claudio
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Univ Zurich, Switzerland.
    Restivo, Gaetana
    Univ Hosp Zurich, Switzerland.
    Hafner, Jurg
    Univ Hosp Zurich, Switzerland.
    Basler, Konrad
    Univ Zurich, Switzerland.
    van den Broek, Maries
    Univ Zurich, Switzerland.
    WNT ligands control initiation and progression of human papillomavirus-driven squamous cell carcinoma2018In: Oncogene, ISSN 0950-9232, E-ISSN 1476-5594, Vol. 37, no 27, p. 3753-3762Article in journal (Refereed)
    Abstract [en]

    Human papillomavirus (HPV)-driven cutaneous squamous cell carcinoma (cSCC) is the most common cancer in immunosuppressed patients. Despite indications suggesting that HPV promotes genomic instability during cSCC development, the molecular pathways underpinning HPV-driven cSCC development remain unknown. We compared the transcriptome of HPV-driven mouse cSCC with normal skin and observed higher amounts of transcripts for Porcupine and WNT ligands in cSCC, suggesting a role for WNT signaling in cSCC progression. We confirmed increased Porcupine expression in human cSCC samples. Blocking the secretion of WNT ligands by the Porcupine inhibitor LGK974 significantly diminished initiation and progression of HPV-driven cSCC. Administration of LGK974 to mice with established cSCC resulted in differentiation of cancer cells and significant reduction of the cancer stem cell compartment. Thus, WNT/beta-catenin signaling is essential for HPV-driven cSCC initiation and progression as well as for maintaining the cancer stem cell niche. Interference with WNT secretion may thus represent a promising approach for therapeutic intervention.

1 - 4 of 4
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