Lab Projects
Cancer Metabolism and EMT Plasticity
Cancer progression is driven not only by genetic mutations, but also by dynamic changes in cell state. One of the most important of these transitions is the epithelial-to-mesenchymal transition (EMT), a process that enables cancer cells to acquire invasive, metastatic, and therapy-resistant properties.
Our lab studies how metabolic processes regulate EMT and epithelial-mesenchymal plasticity (EMP). We investigate how metabolic enzymes, intracellular metabolites, and redox balance shape cancer cell identity and influence signaling pathways that control migration, invasion, metastasis, and treatment response.
By combining CRISPR-based genetic screens, metabolomics, bioinformatics, and in vivo models, we aim to identify metabolic vulnerabilities that can be therapeutically targeted in aggressive cancers.
The role of GPX8 in controlling cancer cell state and metastatic potential
GPX8 is an endoplasmic reticulum-associated glutathione peroxidase that plays a critical role in maintaining intracellular redox balance and regulating cancer cell behavior. Our work has identified GPX8 as a key regulator of cancer cell plasticity, particularly in aggressive tumor subtypes that exhibit mesenchymal features and high metastatic potential.
We found that GPX8 expression is strongly associated with the EMT program and is enriched in highly invasive cancer cells. Loss of GPX8 shifts cancer cells toward a more epithelial state, reduces migration and invasiveness, and alters their response to environmental stress and therapy.
Our research aims to understand how GPX8 controls cell state transitions and how its activity supports tumor progression and metastasis. By studying the molecular pathways regulated by GPX8, we seek to identify new therapeutic strategies for targeting aggressive cancers.
Investigating How Dihydropyrimidines Regulate Cancer Cell State and Aggressiveness
Dihydropyrimidines are intermediate metabolites generated during pyrimidine degradation, yet their role in cancer biology remains largely unexplored. Our lab investigates how these metabolites influence cancer cell state and contribute to tumor aggressiveness.
We study how intracellular accumulation or depletion of dihydropyrimidines affects epithelial–mesenchymal plasticity (EMP), cell migration, and metastatic potential. Our findings suggest that these metabolites are not merely byproducts of metabolism, but active regulators of signaling pathways that shape cancer cell behavior.
By combining metabolic profiling, genetic perturbation, and functional assays, we aim to uncover how pyrimidine metabolism controls cell state transitions and whether these pathways can be exploited as new therapeutic vulnerabilities in aggressive cancers.
EXT1/HSPG axis in cancer cell plasticity
EXT1 (Exostosin Glycosyltransferase 1) is a key enzyme required for heparan sulfate proteoglycan (HSPG) biosynthesis, a process that plays an essential role in regulating how cancer cells sense and respond to their microenvironment. Our lab investigates how the EXT1/HSPG axis controls cancer cell plasticity and promotes aggressive tumor behavior.
We found that EXT1 is selectively upregulated in aggressive tumor subtypes and in cancer cells with strong mesenchymal characteristics. Loss of EXT1 reduces migration, invasion, tumor formation, and metastatic potential, while impairing key signaling pathways associated with cancer progression, particularly STAT3 signaling.
Our research focuses on understanding how HSPG biosynthesis shapes oncogenic signaling and supports epithelial–mesenchymal plasticity (EMP). By studying the EXT1/HSPG/STAT3 axis, we aim to identify new therapeutic opportunities for targeting highly aggressive and therapy-resistant cancers.
DPYSL2 as a Regulator of JAK–STAT3 Signaling and Cancer Cell Plasticity
DPYSL2 (Dihydropyrimidinase-Like 2), also known as CRMP2, is a multifunctional adaptor protein best known for its role in neuronal development, but its function in cancer progression has remained largely unexplored. Our lab investigates how DPYSL2 regulates cancer cell migration, signaling, and metastatic behavior.
We discovered that DPYSL2 plays a central role in controlling cancer cell aggressiveness by regulating the JAK–STAT3 signaling pathway through its interaction with JAK1. Loss of DPYSL2 reduces STAT3 activation, impairs cancer cell migration, and suppresses invasive behavior, highlighting its importance in maintaining aggressive tumor phenotypes.
Our research focuses on understanding how DPYSL2 integrates signaling and metabolic cues to control epithelial–mesenchymal plasticity (EMP) and tumor progression. By uncovering the molecular mechanisms regulated by DPYSL2, we aim to identify new strategies for targeting metastatic and therapy-resistant cancers.