dr. Nicolas Skrypek (PhD)
Post-doctoral researcher - Unit for Molecular Cellular Oncology - Inflammation Research Center (VIB-UGent)
(PI: prof. Geert Berx)
Epithelial-to-mesenchymal transition (EMT) is a process leading to a switch from a polarized epithelial phenotype to a motile and mesenchymal phenotype. EMT is essential for proper embryonic development and also in adult life it is involved in several physiological (e.g. wound healing) and pathological conditions (e.g. fibrosis, cancer progression). In cancer, EMT is described as essential for tumor cells dissemination and in chemoresistance mechanism, two critical properties linked with poor treatment responsiveness and poor prognosis. EMT is tightly regulated by a network of transcription factors that repress epithelial gene expression (e.g. E-cadherin, Occludin) while activating mesenchymal gene expression (e.g. Vimentin). We are focusing on Zinc finger E-box binding homeobox (ZEB) family represented by ZEB1 and ZEB2. Both ZEB factors are overexpressed in several cancer types (e.g. breast, ovarian, colorectal…) correlated with metastasis and a bad prognosis. Our previous and ongoing studies showed that ZEB proteins are regulating specific cellular aspects, However the specific functional activity of ZEB1 and ZEB2 are not well understood, neither as the molecular mechanism by which ZEB factors activate gene transcription. Part of ZEB specific activity is suspected to be through the interaction with co-regulatory complex as epigenetic regulators (e.g. NuRD, LSD1…) or other TFs but the importance of such interactions in ZEB cancer activity needs to be further studied. Using genome-wide techniques (ChIP-seq, RNA-seq, RBBS…) and proteomic data, we want to found the specific partners of either ZEB1 or ZEB2 and their global impact on the genome and epigenome correlated with gene expression and EMT.
Contact and links
- Unit for Molecular Cellular Oncology - Inflammation Research Center (VIB-UGent), Technologiepark 71, 9052 Zwijnaarde-Gent
- LinkedIn profile