Metastases cause over 90% of cancer deaths, yet targeted therapies remain elusive. As they often emerge after surgery, preventing them through neoadjuvant or adjuvant treatments is a promising strategy. However, the lack of therapies directly targeting the metastatization process poses a major challenge, making it crucial to unravel its molecular mechanisms for innovative treatments.
In the genome of normal human breast epithelial cells, we recently identified >1,000 hotspots of DNA damage, which are bound by (DNA-repair proteins and) GRHL2, a master epithelial transcription factor and suppressor of epithelial-to-mesenchymal transition, a key driver of metastasis.
GRHL2 is essential for both DNA damage accumulation and activity of these regions, which function as enhancers that regulate the expression of distant key epithelial genes through DNA looping with their promoters.
We propose that the persistent generation and repair of DNA damage at these genomic regions bound by epithelial-determining transcription factors generates chromosomal instability in epithelial cancers. Specifically, we hypothesize that GRHL2 binding to target enhancers induces DNA damage and triggers the recruitment of DNA-repair proteins. This process may promote local genomic rearrangements, disrupting enhancer-promoter interactions, weakening the epithelial transcriptional program, and ultimately driving the transition toward mesenchymal and metastatic phenotypes.
This project has the potential for significant impact on biomedical research at multiple levels: i) it will provide insights into fundamental transcriptional regulation mechanisms in three-dimensional nuclear architecture; ii) it will allow the identification of molecular events in primary tumors that drive metastasis, thus revealing biomarkers for patient stratification (enhancer-associated mutations or deregulation of the target genes) and new therapeutic targets to inhibit metastatization, ultimately reducing breast cancer mortality.
This project is funded by the Italian Ministry of University and Research (MUR) under the Fondo Italiano per la Scienza (FIS 3) programme.
Posted on November 06, 2026