My research interest is to understand the molecular basis of carcinogenesis, cancer development and chemo-/radio-resistance, with a focus on cancer metabolism, reactive oxygen species, epigenetic regulation on signaling pathways. We are also interested in how these processes prime tumor microenvironment to favor tumor growth. Our ultimate goal is to personalize cancer therapy by uncovering novel druggable targets to improve therapeutic efficiency.
S6K1 in acquired resistance to EGFR-TKI in NSCLC
Abnormal oncogenic activation of EGFR signaling is a key trigger in various cancers, and application of small molecule tyrosine kinase inhibitors has provided benefit for lung cancer patient. However, in spite of initial response, all responding patients eventually developed acquired resistance to EGFR-TKIs. This study is to investigate the roles of ribosomal protein S6 kinase 1(S6K1) on the acquired resistance to EGFR-targeted therapy in NSCLCs that do not harbor secondary EGFR mutations.
Heavy metal-induced carcinogenesis
Environmental and occupational exposure to heavy-metal is a major public health concern. Our lab mainly investigates the molecular mechanisms including epigenetic regulation and metabolic reprogramming underlying the arsenic- and chromium VI-induced cell malignant transformation and carcinogenesis through in vitro, in vivo experiments, and population-based study
Tumor exosomal miRNAs in ovarian cancer development
Tumor-derived exosomes are emerging mediators of tumorigenesis within the tumor microenvironment. As the first classes of nucleic acids identified in exosomes, miRNAs are enriched in exosomes, and have been revealed to be functional and can impact recipient cells. In this project, we aim to study how tumor exosomal miRNAs affect immune cells and vascular endothelial cells, which eventually boosts tumor angiogenesis and metastasis in ovarian cancer.