title: Melanoma cells revive an embryonic transcriptional network to dictate phenotypic heterogeneity.
abstract: Compared to the overwhelming amount of literature describing how epithelial-to-mesenchymal transition (EMT)-inducing transcription factors orchestrate cellular plasticity in embryogenesis and epithelial cells, the functions of these factors in non-epithelial contexts, such as melanoma, are less clear. Melanoma is an aggressive tumor arising from melanocytes, endowed with unique features of cellular plasticity. The reversible phenotype-switching between differentiated and invasive phenotypes is increasingly appreciated as a mechanism accounting for heterogeneity in melanoma and is driven by oncogenic signaling and environmental cues. This phenotypic switch is coupled with an intriguing and somewhat counterintuitive signaling switch of EMT-inducing transcription factors. In contrast to carcinomas, different EMT-inducing transcription factors have antagonizing effects in melanoma. Balancing between these different EMT transcription factors is likely the key to successful metastatic spread of melanoma.
authors.affiliation: Unit of Molecular and Cellular Oncology, Inflammation Research Center , VIB, Ghent , Belgium ; Department of Biomedical Molecular Biology, Ghent University , Ghent , Belgium.
authors.forename: Niels
authors.initials: N
authors.lastname: Vandamme
authors.affiliation: Unit of Molecular and Cellular Oncology, Inflammation Research Center , VIB, Ghent , Belgium ; Department of Biomedical Molecular Biology, Ghent University , Ghent , Belgium.
authors.forename: Geert
authors.initials: G
authors.lastname: Berx
keywords: EMT; MITF; SLUG; ZEB1; ZEB2; drug-resistance; melanoma; phenotype-switching