Ming Chen
Principal Investigator
Associate Professor in Pathology
Associate Research Professor of Cell Biology
Member of the Duke Cancer Institute
Contact Information


Duke Box 103863
Department of Pathology
Duke University School of Medicine
Durham, NC 27710

Research Interests

Research in the Chen laboratory mainly focuses on three areas:

(1) Mechanisms of Metastasis

Metastasis accounts for more than 90% of cancer-related deaths and yet remains one of the least understood aspects in cancer biology. One objective in our research is to identify mechanisms of metastasis and vulnerability of metastatic cells. We are among few groups that generate mouse models of metastatic prostate cancer based on prostate epithelium-specific inactivation of Pten. By performing integrative omics analyses of tumors from localized and metastatic mouse models, we aim to reveal transcriptional, translational and metabolic mechanisms that drive metastatic disease. Additionally, by conducting preclinical studies of drugs targeting vulnerability of metastatic cells, we hope we can find new strategies to prevent or slow the cancer spread in mice, and maybe eventually translate into the clinic.

(2) Lipid Metabolism and Cancer

Cancer cells are known to undergo metabolic reprogramming to support their rapid proliferation and growth. One of the most frequently dysregulated metabolic pathways in cancer is the activation of de novo lipogenesis. Our recent studies suggest that co-activation of the PI3K/AKT and MAPK pathways converges their oncogenic functions through SREBP-dependent lipogenic program, and that lipids obtained through de novo lipogenesis or dietary uptake may provide a cell-intrinsic signal promoting the aggressiveness of cancer. A current focus in the lab is to identify key genes and pathways that mediate lipid-driven tumorigenesis and to establish the molecular mechanisms connecting obesity and aggressive cancer.

(3) PTEN/PI3K/AKT and MAPK Signaling in Cancer

PTEN/PI3K/AKT and MAPK signaling pathways govern a variety of biological processes, including cell survival, proliferation, growth and metabolism. They are the most commonly altered pathways in human cancer and their cross-talk is also of key importance in the regulation of tumorigenesis. We have recently revealed a PP1α-PML molecular network that is genetically altered in human cancer towards aberrant MAPK activation in PTEN loss/PI3K-AKT driven cancers. Our studies are now focused on developing optimal combinatorial therapies that target different components of the pathway to combat human cancer.


Please see a complete list of published works at PubMed.

Book Sections

Journal Articles