Research Projects

Epithelial mesenchymal plasticity (EMP) is a cellular program linked to metastasis initiation and therapy resistance. It generates non-genetically heterogeneous cell populations, including epithelial (E), mesenchymal (M), and hybrid epithelial mesenchymal (h E/M) cells. During the E to M transition, E cells lose cell-cell adhesion, allowing them to form metastatic tumors. Transcriptional regulatory networks (TRNs) under EMP have been identified and linked to tumor heterogeneity and metastasis initiation ability. Cell-cell signaling events also play a crucial role in cell fate choice determination. This work proposes a comprehensive higher-order stability analysis of EMP networks, mapping distinct stable states to corresponding biological phenotypes (E, h1/h2-E/M, and M). It aims to identify topological signatures that stabilize E, M, and h E/M phenotypes and enable transitioning between them. The integrated approach will provide insights into molecular signatures regulating cell fate transition, leading to the identification of inhibitors of phenotypic transition and tumor heterogeneity.