We interrogate crosstalks between cancer cells and the microenvironment in metastatic colorectal and pancreatic cancers. For example, the surrounding liver mcrienvironment secretes soluble factors to activate HER3 and other survival pathways in cancer liver metastases. By identifying key survival pathways (such as HER3) ivolved in the crosstalk, we aim to develop therapeutic strategies of disrupting the crosstalk (e.g. block secreted factors, or block HER3 in cancer cells) to inhibit metastatic tumor outgrowth and, and also sensitize cancer cells to standard-of-care treatments for combination therapies.
Research Information
Research Interests
My laboratory aims to understand how the microenvironment, both intratumoral and the surrounding host organs, mediates cancer cell growth and chemoresistance in colorectal and pancreatic cancers. We establish patient-derived primary cells from malignant and non-malignant tissues (human and murine) to elucidate cancer-stromal cell crosstalk and key mediating pathways for developing new anti-neoplastic regimens. We recently identified liver-secreted LRG1 as a novel HER3 ligand and promote growth and survival in colorectal cancer liver metastases (Gastroenterology, 2024. PMID: 39393543).
We are also interested in understanding the development of inflammatory bowel diseases, with a focus on identifying key disease-driving pathways in immune and epithelial cells in the intestinal mucosa.
Current Projects
- Determine the paracrine effects of the surrounding liver parenchyma on metastatic colorectal and pancreatic cancer survival
- Elucidate roles of canonical and noncanonical HER3 signaling pathways in regulating survival and metabolic reprogramming in metastatic colorectal and pancreatic cancer
- Single cell- and spatial -omics analysis to characterize distinct tumor microenvironment components in primary and metastatic tumors
- Determine HER3- and NPTX2-mediated inflammatory responses in immune and epithelial cells in inflammatory bowel diseases.