Doctoral fellow - Unit of Molecular and Cellular Oncology - Inflammation Research Center, VIB
Doctoral fellow - Department of Biomedical Molecular Biology - Ghent University
(PI: prof. Geert Berx)
The melanocyte lineage originates from the embryonic neural crest. During cell fate specification, the neural crest cells undergo epithelial to mesenchymal transition (EMT). During EMT, epithelial cells lose their epithelial traits and gain mesenchymal traits, becoming motile cells. As such melanocytes can be regarded as a mesenchymal product of EMT. In non-epithelial context such as melanoma, the role of EMT-inducing transcription factors is less well understood. Melanoma cells have the ability to reversibly switch their phenotype between a differentiated and an invasive phenotype, the 'phenotype-switching model'. It has been shown that reversible switching of the EMT master regulators ZEB1 and ZEB2, plays a key role in this cellular plasticity of melanoma cells. However, the molecular mechanism by which these transcription factors function during melanocyte lineage differentiation and melanoma phenotype-switching is not well understood.
ZEB2 is a multi-domain transcription factor that interacts with other co-factors in a context-dependent manner to perform diverse functions. It is of great interest to know which specific biological function ZEB2 has, depending on the protein complex it is present in. As such, we want to identify interaction partners of ZEB2 in both melanocyte and melanoma cell lines and determine their role during melanocyte differentiation and melanoma progression. Next, we want to determine the epigenetic role of ZEB2 or its interaction partners in melanoma.
Contact and links
- Geert Berx lab
- address: Technologiepark 927, 9052 Zwijnaarde - Belgium