Emory School of Medicine
Dr. Li obtained his Medical Degree from the Xiang-Ya Medical college in 1985 and completed his graduate program training at the Peking Union Medical College (1991). He completed his postdoctoral training in Dr. Varda Rotter’s laboratory at the Weizmann Institute of Science and then in Dr. Takis Papas’ laboratory at the Medical University of South Carolina. Dr. Li was appointed Assistant Professor in 2004 in the Department of Pathology and Laboratory Medicine at the Medical University of South Carolina and then Assistant Professor in 2008 at Emory University. Dr. Li is credited as the first to demonstrate that the mutation of p53, a tumor suppressor gene, significantly interferes with chemotherapy-induced apoptosis (1997), which provides important information for successful anti-cancer chemotherapy. Dr Li’s work on ETS1 and its associated proteins has provided a better understanding of the role of ETS1 in tumorigenesis and metastasis, and he is also credited with the discovery and cloning of the novel genes EAPI/Daxx (2000) and EAPII/TTRAP/TDP2 (2003). Dr. Li is a recipient of the NIH career development award (K22).
Dr. Li’s research focuses on the tumor microenvironment and metastasis, and in particular, he studies the mechanisms of how diverse microenvironmental signals, including cytokines, growth factors, and cellular stresses, regulate tumor formation and progression. The ongoing projects in Dr. Li’s laboratory are:
1) Elucidating the tumor microenvironmental signals that modulate ETS1, a proto-oncogene and founding member of the Ets gene family. ETS1 functions as a transcription factor and plays important roles in lymphocyte development, invasiveness, and angiogenesis. Determination of how ETS1 activity is modulated in response to extracellular signals and subsequently regulates cancer progression-related genes will reveal novel targets for tumor microenvironment intervention.
2) Characterizing the mechanisms by which EAPII contributes to tumorigenesis and chemoresistance. EAPII is a novel protein which interacts with ETS1. Dr Li’s group discovered and characterized EAPII as a negative modulator of the ETS1 transcription factor (2003). Recently, he identified the oncogenic role of EAPII in lung cancer development (2011). Emerging data suggest that EAPII is a pleiotropic functional protein: EAPII repairs enzyme (topoisomerase)-mediated DNA damage by removing phosphotyrosine from DNA adducts; EAPII is involved in multiple signal transduction pathways such as TNF-TNFR, TGFb, and MAPK; and EAPII is responsive to immune defense, inflammatory response, virus infection, and DNA toxic (chemo or radiation therapy).
Currently. Dr. Li’s team is determining the mechanisms by which EAPII plays pleiotropic functions in tumor formation and chemoresistance. Ultimately, his studies will provide a potential novel target for cancer intervention.
View publications on PubMed