In this project, we are using cell-line models of epithelial-mesenchymal transition (EMT) to identify the molecular interactions and regulatory networks that underpin EMT in breast cancer.

To date, we have discovered that different triggers of EMT cause substantially different molecular responses, and use different signalling networks to drive toward a convergent phenotype. We have also identified distinctive differences in the way cell line models respond to drugs, depending on whether their EMT is triggered by signalling molecules or hypoxia.

This work is part of the EMPathy Breast Cancer Network.

Team members: Sepideh Foroutan, Soroor Zadeh