Cytoskeleton and Cell Plasticity
Campus Limpertsberg, 162a, avenue de la Faïencerie, L-1511 Luxembourg
Phone: +352 46 66 44 65 81
Inflammation-driven biological processes such as wound-healing, fibrosis or carcinoma progression rely on the capacity of epithelial cells to acquire a mesenchymal phenotype (Epithelial to Mesenchymal Transition; EMT) via genetic reprogramming. Involving also enhanced migration, this process strongly implicates the actin cytoskeleton, a dense meshwork of protein filaments undergoing rapid cycles of assembly and disassembly in cells. This dynamic structure defines the architecture of epithelial cells and participates in key cell processes like endocytosis, cytokinesis, cell migration and signalling. More recently, a nuclear function was identified for actin in the organisation of chromatin and gene expression. Since structural and functional alterations of the actin cytoskeleton are associated with EMT, this complex structure is a potential target for novel anti-cancer therapies.
We combine microscopy-based quantitative live cell imaging, biochemical and OMICS approaches with mathematical modelling 1) to gain an integrated view on the assembly of cytoskeleton structures in the context of the epithelial cell, 2) to understand how actin polymerization contributes to cell motility 3) In parallel, we investigate gene regulatory circuits including small non-coding microRNAs, which contribute to the regulation of epithelial cell plasticity. These approaches will allow unravelling the molecular bases of fundamental biological events which contribute to inflammation-based diseases.
1) Systematic study of early stage gene regulatory networks including miRNA-orchestrated events, during carcinoma progression (FNR BIOSAN, UL internal and FLCC projects):
2) Investigation of the spatio-temporal regulation of the assembly of actin structures involved in cell migration and morphogenesis (UL internal project):