Cancer Biology
Tumor-Host Cell Interactions
A critical step in cancer metastasis is intravasation, during which tumor cells cross the endothelial barrier to enter the circulation. While this barrier has traditionally been viewed as a passive physical obstacle, emerging evidence suggests that tumor cells actively engage and remodel endothelial cells to facilitate dissemination.
Our work examines transcellular migration pathways in which tumor cells pass directly through endothelial cells, forming transient cell-in-cell–like structures. Using co-culture systems, live-cell imaging, and single-cell analyses, we uncovered a previously unrecognized mode of tumor–endothelial interaction characterized by the formation of double-positive cells and extensive intercellular exchange. These interactions are accompanied by the transfer of genetic material between cells, a process we term Tangocytosis.
Current efforts focus on defining the molecular mechanisms underlying Tangocytosis, determining its functional consequences for metastatic competence, and understanding how direct tumor–endothelial communication actively shapes metastatic intravasation.
Redox Regulation, Epigenetic Stress, and Tumor Cell Fate
In parallel, the lab investigates how tumor cells respond to oxidative and epigenetic stress and how these responses influence survival, drug sensitivity, and immune engagement. A major focus of this work is the multifunctional enzyme peroxiredoxin-6 (PRDX6), which plays a central role in redox homeostasis and lipid metabolism.
We study how PRDX6 activity supports tumor cell resilience by buffering oxidative stress and preventing stress-induced cell death. Disrupting PRDX6 function sensitizes cancer cells to epigenetic perturbations, including histone deacetylase (HDAC) inhibition with compounds such as largazole and OKI-179. Using chemical, genetic, and imaging approaches, we examine how combined redox and epigenetic stress reshapes tumor cell fate decisions, promotes ferroptotic and inflammatory cell death pathways, and enhances anti-tumor immune responses.
Ongoing work aims to define how redox control and chromatin regulation intersect to govern tumor vulnerability and to identify therapeutic strategies that exploit these dependencies in cancer.