Our laboratory focuses on the fundamental and translational mechanisms governing tumor initiation, progression, and metastasis, with a particular emphasis on pancreatic ductal adenocarcinoma (PDAC)—one of the most lethal malignancies. We aim to understand how tumor cells adapt to microenvironmental stress and how these adaptations reshape the tumor ecosystem to drive disease progression and therapeutic resistance. To address these questions, we integrate multidisciplinary approaches spanning cell biology, cancer biology, and systems biology. Our experimental platforms include cancer cell lines, genetically engineered and xenograft mouse models, as well as patient-derived tissues and organoid systems. We combine CRISPR-based functional genomics, single-cell and spatial multi-omics, and AI-assisted drug discovery to uncover actionable vulnerabilities and accelerate therapeutic development. Our work has been published in leading journals such as Nature Cell Biology, Blood, Advanced Science, Trends in Cell Biology, and Oncogene.

Key research interests:

1.Tumor Microenvironment and ECM Remodeling

We investigate how cancer-associated fibroblasts (CAFs), immune cells, and extracellular matrix (ECM) components dynamically interact with tumor cells to shape tumor evolution. A central goal is to define how ECM remodeling and stromal signaling regulate tumor cell plasticity, stemness, and therapy resistance.

2.Stress Adaptation and Tumor Cell Plasticity

Tumor cells are constantly exposed to microenvironmental stresses, including hypoxia, nutrient deprivation, and therapeutic pressure. We study how stress-responsive membrane proteins and signaling pathways enable cancer cells to adapt, survive, and acquire aggressive phenotypes. We further explore strategies to disrupt these adaptive programs for therapeutic benefit.

3.Target Discovery and Translational Therapeutics

We seek to identify and validate novel molecular targets that drive tumor progression and resistance. Leveraging AI-guided drug discovery, we develop small molecules, peptides, and antibody-based therapeutics aimed at targeting tumor–stroma interactions and stress-adaptive signaling pathways, with the ultimate goal of advancing precision oncology.

Our long-term goal is to bridge fundamental cancer biology with clinical translation by identifying key regulatory nodes within the tumor microenvironment and stress-response networks, and by developing mechanism-driven therapeutic strategies to improve outcomes for patients with PDAC and other solid tumors.

• Stress-responsive membrane proteins as execution nodes of tumor cell adaptation to microenvironmental stress. Oncogene. 2026
• Therapeutic targeting of Toll-like receptor pathways in tumor-associated macrophages. Cytokine & Growth Factor Reviews. 2026
• HSP90AB1-mediated ubiquitin-proteasome degradation of ITGBL1 promotes osteosarcoma progression by inhibiting endoplasmic reticulum stress-induced autophagy. Advanced Science. 2026
• Targeting pancreatic cancer cell stemness by blocking fibronectin-binding integrins on cancer-associated fibroblasts. Cancer Research Communications. 2025
• Tumor-initiating cells establish a niche to overcome isolation stress.  Trends in Cell Biology. 2024   
• Integrin αvβ3 Upregulation in Response to Nutrient Stress Promotes Lung Cancer Cell Metabolic Plasticity. Cancer Research. 2024  
• Upregulation of fibronectin and its integrin receptors - an adaptation to isolation stress that facilitates tumor initiation. Journal of Cell Science. 2023  
• Pancreatic cancer cells upregulate LPAR4 in response to isolation stress to promote an ECM-enriched niche and support tumour initiation.  Nature Cell Biology.  2023  
• Metabolic Reprograming via Deletion of CISH in Human iPSC-Derived NK Cells Promotes In Vivo Persistence and Enhances Anti-tumor Activity. Cell Stem Cell.  2020  
• Oxidative stress enhances tumorigenicity and stem-like features via the activation of the Wnt/β-catenin/MYC/Sox2 axis in ALK-positive anaplastic large-cell lymphoma. BMC Cancer. 2018 
• A positive feedback loop involving the Wnt/β-catenin/MYC/Sox2 axis defines a highly tumorigenic cell subpopulation in ALK-positive anaplastic large cell lymphoma. Journal of Hematology and Oncology. 2016 
• The PI3K/AKT/c-MYC axis promotes the acquisition of cancer stem-like features in esophageal squamous cell carcinoma. Stem Cells. 2016 
• STAT1 is phosphorylated and downregulated by the oncogenic tyrosine kinase NPM-ALK in ALK-positive anaplastic large-cell lymphoma. Blood. 2015