Research Program

Metastasis is an extreme stress test for cancer cells. To survive dissemination, circulation, colonization and therapy, metastatic cells must adapt to oxidative, metabolic, and microenvironmental stress. Our lab studies the mechanisms that enable this adaptation, with a particular focus on translational remodeling, RNA biology, and stress-response signaling. We aim to define the molecular programs that allow metastatic cells to survive hostile environments and to identify the vulnerabilities these programs create.

Building on foundational work showing that oxidative stress limits metastatic spread, we investigate how cancer cells rewire gene expression and metabolism to survive under conditions of redox imbalance, hypoxia and nutrient limitation. Across these projects, our goal is to uncover mechanisms that are not only biologically central to metastatic progression and therapy resistance, but also therapeutically actionable.

Current Research Themes

  • Oxidative and Metabolic Adaptations

    Metastatic cells encounter profound oxidative and metabolic stress during dissemination, circulation, and organ colonization. We study how cancer cells reprogram metabolism and antioxidant defenses to survive these challenges, adapt to distinct tissue environments, and establish metastatic lesions. This work aims to define how stress adaptation support metastatic fitness and plasticity and where it creates selective vulnerabilities that can be targeted therapeutically.

  • Selenoprotein Translation and Redox Control

    Many of the enzymes that protect cells from oxidative damage depend on selenocysteine, a specialized amino acid incorporated through an unusual translational mechanism. We investigate how the selenoproteome is regulated in metastatic cells and how this program supports oxidative stress resistance. By studying selenoprotein translation in metastasis, we aim to uncover mechanisms that connect translational control to redox homeostasis and cancer cell survival.

  • tRNA Modifications and Stress-Responsive Translation

    Metastatic cells must rapidly adjust protein synthesis as they encounter changing microenvironments and therapeutic stress. We study how tRNA levels, tRNA modifications, codon-biased translation, and stress-responsive translational programs shape the adaptive proteome in metastatic disease. This work focuses on how RNA-level regulation enables phenotypic plasticity, promotes survival under stress, and creates opportunities for therapeutic intervention.