• Wei-Xing Zong
  • Wei-Xing Zong
  • Professor
  • Department: Department of Chemical Biology
  • Program(s): Cell and Developmental Biology Graduate Program, Cellular and Molecular Pharmacology Graduate Program
  • Rotating Faculty
  • Phone: 1.8484454940
  • Rutgers University
  • Ernest Mario School of Pharmacy
  • Susan Lehman Cullman Laboratory for Cancer Research, Room 215
  • 164 Frelinghuysen Road
  • Piscataway, NJ 08854
  • Key Words: Cancer Metabolism, Protein Homeostasis, Redox Regulation, Autophagy, Cell Death

Cancer Cell Metabolism and Growth Signaling

The research in my laboratory focuses on the regulation of protein and metabolic homeostasis during oncogenesis and cancer therapy. We study apoptosis, autophagy, ER stress, ROS, and metabolism. We use mostly biochemical, molecular biological, and cell biological methodologies, as well as genetically engineered mouse models and clinical samples.

1. Proteotoxic stress and signaling
Many cell types including cancer cells are often under the stress of misfolded proteins that leads to many molecular consequences such as increased reactive oxygen species (ROS), unfolded protein response signaling, and cell death. Inhibition of protein degradation is an emerging anti-cancer strategy. A major line of research in the lab is to understand the mechanisms underlying these molecular events. Ongoing projects involve the regulation of redox homeostasis by the ubiquitin E3 ligase TRIM21, and the regulation of cell death via p62-mediated caspase-8 aggregation.

2. Oncogenic regulation of protein and bioenergetics homeostasis
We study how phosphatidylinositol 3-kinases (PI3Ks) regulate autophagy and endocytosis, and how these functions are involved in oncogenesis. Another line of research in the lab is to understand how PI3-kinases and c-Myc oncogenes regulate cancer cell metabolism.

3. Cancer metabolism
Metabolic programs are known to be altered in cancers arising from various tissues. Malignant transformation can alter signaling pathways related to metabolism and increase the demand for both energy and biomass for the proliferating cancerous cells. This scenario is further complexed by the crosstalk between transformed cells and the microenvironment. My lab studies how oncogenes regulate the reprogramming of cancer cell metabolism, and how the metabolic changes impact oncogenesis with the attempt to harness it for cancer therapy.

 

Publications