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Melanoma cells revive an embryonic transcriptional network to dictate phenotypic heterogeneity

By Niels eVandamme, Niels eVandamme and Geert eBerx and Geert eBerx


Compared to the overwhelming amount of literature describing how epithelial-to-mesenchymal (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

Topics: Melanoma, EMT, drug-resistance, Slug, MITF, phenotype switching, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Publisher: Frontiers Media S.A.
Year: 2014
DOI identifier: 10.3389/fonc.2014.00352
OAI identifier: oai:doaj.org/article:caab440644684b4392ce43768a284e40
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