Nature Communications (Aug 2021)
Epigenetic control of melanoma cell invasiveness by the stem cell factor SALL4
- Johanna Diener,
- Arianna Baggiolini,
- Mattias Pernebrink,
- Damian Dalcher,
- Luigi Lerra,
- Phil F. Cheng,
- Sandra Varum,
- Jessica Häusel,
- Salome Stierli,
- Mathias Treier,
- Lorenz Studer,
- Konrad Basler,
- Mitchell P. Levesque,
- Reinhard Dummer,
- Raffaella Santoro,
- Claudio Cantù,
- Lukas Sommer
Affiliations
- Johanna Diener
- University of Zürich, Institute of Anatomy
- Arianna Baggiolini
- University of Zürich, Institute of Anatomy
- Mattias Pernebrink
- Wallenberg Centre for Molecular Medicine, Linköping University
- Damian Dalcher
- University of Zürich, Department of Molecular Mechanisms of Disease
- Luigi Lerra
- University of Zürich, Department of Molecular Mechanisms of Disease
- Phil F. Cheng
- University Hospital of Zürich, Department of Dermatology
- Sandra Varum
- University of Zürich, Institute of Anatomy
- Jessica Häusel
- University of Zürich, Institute of Anatomy
- Salome Stierli
- University of Zürich, Institute of Anatomy
- Mathias Treier
- Max-Delbrück-Center for Molecular Medicine
- Lorenz Studer
- Developmental Biology, The Center for Stem Cell Biology, Memorial Sloan Kettering Cancer Center
- Konrad Basler
- University of Zürich, Institute of Molecular Life Sciences
- Mitchell P. Levesque
- University Hospital of Zürich, Department of Dermatology
- Reinhard Dummer
- University Hospital of Zürich, Department of Dermatology
- Raffaella Santoro
- University of Zürich, Department of Molecular Mechanisms of Disease
- Claudio Cantù
- Wallenberg Centre for Molecular Medicine, Linköping University
- Lukas Sommer
- University of Zürich, Institute of Anatomy
- DOI
- https://doi.org/10.1038/s41467-021-25326-8
- Journal volume & issue
-
Vol. 12,
no. 1
pp. 1 – 18
Abstract
Melanoma cells can switch between proliferative and invasive phenotypes. Here the authors show that the embryonic stem cell factor Sall4 is a negative regulator of melanoma phenotype switching where its loss leads to the acquisition of an invasive phenotype, due to derepression of invasiveness genes.
