Date:  12 Nov 2026 (Thurs)
Time: 3:30-4:30 pm
Venue: Seminar Room 2&3, Laboratory Block, 21 Sassoon Road
Host: Professor Kathryn Cheah

Ángela Nieto is Full Professor at the Institute of Neurosciences, a joint center of the Spanish National Research Council (CSIC) and Miguel Hernández University in Alicante, Spain. She directs the Cellular Plasticity in Disease and Brain Repair program and coordinates the CSIC National Cancer Hub. After completing her PhD at the Centro de Biología Molecular Severo Ochoa (Madrid), she pursued research at the Max Planck Institut für Psychiatrie in Munich and at the National Institute for Medical Research in London before establishing her independent group at the Cajal Institute in Madrid in 1993. She moved with her whole group to Alicante in 2004. Her work focuses on cellular plasticity in development and disease, with major contributions to understanding how reactivation of developmental programs drives cancer progression and organ degeneration. She is a member of the Spanish and European Academies of Sciences and a foreign member of the French and Latin American Academies. Her awards include the Mexico Prize (2017), Spain’s National Research Award (2019), and the L’Oréal-UNESCO For Women in Science Award (Europe 2022).

Epithelial homeostasis is crucial for maintaining tissue architecture and must therefore be tightly regulated in the adult. In contrast, embryonic cells show a high degree of epithelial plasticity necessary for proper morphogenesis and for the massive cell movements that occur many developmental processes.

We have studied cell movements and epithelial plasticity, epithelial to mesenchymal transitions (EMT) in particular, and found that the aberrant activation of EMT programs in adult cells leads to several pathologies including tumor progression and organ degeneration. We have developed animal models and performed lineage tracing and single-cell transcriptomics in different settings: the embryonic EMT program implemented during neural crest development and the adult programs activated during either organ fibrosis or cancer.  In fibrosis, we find that inhibiting EMT attenuates the disease in animal models, holding promise for new antifibrotic therapeutic approaches. In cancer, tumor cells that activate EMT bifurcate into two distinct and antagonistic cellular trajectories in segregated populations. Interestingly, these two trajectories correspond to the activation of the embryonic neural crest-like and the adult fibrotic-like EMTs to, respectively, drive dissemination towards metastasis formation or anti-tumor inflammation. Our data on the role for EMT in orchestrating an additional layer of intratumoral heterogeneity suggest its potential in the development of targeted therapies aimed at limiting metastasis and enhancing antitumor immune responses in cancer patients. In summary, understanding how cellular plasticity programs are implemented along trajectories in different pathological contexts provides a suitable platform to design better therapeutic strategies for devastating diseases such as cancer and organ degeneration.

All are welcome.