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Cantù, Claudio
Publications (4 of 4) Show all publications
Fugazza, C., Barbarani, G., Elangovan, S., Marini, M. G., Giolitto, S., Font-Monclus, I., . . . Ronchi, A. E. (2020). The Coup-TFII orphan nuclear receptor is an activator of the γ-globin gene. Haematologica
Open this publication in new window or tab >>The Coup-TFII orphan nuclear receptor is an activator of the γ-globin gene
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2020 (English)In: Haematologica, ISSN 0390-6078, E-ISSN 1592-8721Article in journal (Refereed) Epub ahead of print
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.

Place, publisher, year, edition, pages
Ferrata Storti Foundation, 2020
Keywords
Hemoglobinopathies, Red Cells, Thalassemia
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-164345 (URN)10.3324/haematol.2019.241224 (DOI)32107331 (PubMedID)
Available from: 2020-03-18 Created: 2020-03-18 Last updated: 2020-03-18
Varum, S., Baggiolini, A., Zurkirchen, L., Atak, Z. K., Cantù, C., Marzorati, E., . . . Sommer, L. (2019). Yin Yang 1 Orchestrates a Metabolic Program Required for Both Neural Crest Development and Melanoma Formation. Cell Stem Cell, 24(4), 637-653.e9
Open this publication in new window or tab >>Yin Yang 1 Orchestrates a Metabolic Program Required for Both Neural Crest Development and Melanoma Formation
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2019 (English)In: Cell Stem Cell, ISSN 1934-5909, E-ISSN 1875-9777, Vol. 24, no 4, p. 637-653.e9Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Cell Press, 2019
Keywords
YY1, development, melanoma, metabolism, neural crest, protein synthesis, tumor initiation
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-164344 (URN)10.1016/j.stem.2019.03.011 (DOI)000463353000017 ()30951662 (PubMedID)2-s2.0-85063349622 (Scopus ID)
Available from: 2020-03-18 Created: 2020-03-18 Last updated: 2020-03-24Bibliographically approved
Zimmerli, D., Cecconi, V., Valenta, T., Hausmann, G., Cantù, C., Restivo, G., . . . van den Broek, M. (2018). WNT ligands control initiation and progression of human papillomavirus-driven squamous cell carcinoma. Oncogene, 37(27), 3753-3762
Open this publication in new window or tab >>WNT ligands control initiation and progression of human papillomavirus-driven squamous cell carcinoma
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2018 (English)In: Oncogene, ISSN 0950-9232, E-ISSN 1476-5594, Vol. 37, no 27, p. 3753-3762Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2018
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-149856 (URN)10.1038/s41388-018-0244-x (DOI)000437975200011 ()29662191 (PubMedID)
Note

Funding Agencies|Swiss National Science Foundation (SNF); Swiss Cancer League; Promedica Foundation Zurich; University of Zurich Research Priority Program "Translational Cancer Research"; Kanton of Zurich

Available from: 2018-08-02 Created: 2018-08-02 Last updated: 2018-08-20
Pagella, P., Cantù, C. & Mitsiadis, T. A. (2017). Linking dental pathologies and cancer via Wnt signalling. OncoTarget, 8(59), 99213-99214
Open this publication in new window or tab >>Linking dental pathologies and cancer via Wnt signalling
2017 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 8, no 59, p. 99213-99214Article in journal, Editorial material (Refereed) Published
Place, publisher, year, edition, pages
IMPACT JOURNALS LLC, 2017
Keywords
Bcl9, Wnt signalling, cancer, enamel, tooth
National Category
Cell and Molecular Biology Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-150051 (URN)10.18632/oncotarget.22281 (DOI)000419561600006 ()29245891 (PubMedID)
Available from: 2018-08-08 Created: 2018-08-08 Last updated: 2019-05-16Bibliographically approved
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