POSTDOCTORAL POSITION IN GROWTH AND METABOLIC REGULATION IN CANCER
Postdoctoral opportunities are available to study the control of growth and metabolism in eukaryotes, and the role in cancer and other human diseases. Through genetic and genomic approaches in model organisms, we have identified a large panel of genes involved in these processes. Our current efforts are directed at understanding their functions in normal physiology and diseases in yeast, cultured human cells/organoids, genetically engineered mice and patient samples. Projects in the lab include:
Nutrient Signaling and Human Diseases: Cell growth is a process of assimilating extracellular nutrients such as amino acids and converting them into cell mass. Nutrients are not only basic cell building blocks, but also key chemical signals dictating cell growth and metabolism. mTOR has emerged as a central regulator of cell growth and metabolism in response to nutrient signals. We are using yeast and animal cells as models to tease out key steps in nutrient sensing, growth regulation and malignant growth. Aberrant nutrient signaling is a key contributor to diverse human diseases. For example, poor control of nutrient homeostasis is a major cause for cancer, diabetes, obesity and cardiovascular diseases. We are further investigating how aberrant nutrient signaling results in hyper-activation of mTOR pathway and promote pathological changes such as oncogenic transformation.
Metabolic Stress and Cancer: During cell energy metabolism, by-products known as reactive oxygen species (ROS) are produced. ROS oxidizes macromolecules such as DNA and protein and causes metabolic stressThe cell has developed the ability to sense ROS level, and to closely coordinate metabolic activity and cellular defense mechanisms against ROS. We recently discovered SOD1 as a stress activated transcription factor that regulates diverse antioxidant genes. We are investigating the mechanisms by which the cell coordinates cell metabolism and oxidative stress response under different environmental and pathological conditions. Due to elevated metabolic activity, cancer cells produce very high levels of ROS. Thus they are highly dependent on anti-oxidative mechanisms for survival. We are currently developing new anticancer strategies to explore this vulnerability of human malignancies.
mTOR-targeted Therapy: mTOR forms two distinct protein complexes mTORC1 and TORC2, regulating cell growth and survival, respectively. mTOR pathway is frequently hyper-activated in human cancers, rendering oncogenic advantages in growth and survival. We are interested in understanding how cancer patients respond differently to mTOR inhibitors. Through a better understanding of the genetic and molecular basis of drug sensitivity and resistance, we hope to develop personalized treatment of cancer patients with TOR-targeted therapeutics.
Samples of our recent publications include: Hepatology, (2016) 63:1928; Cell Reports (2015) 11:446; Cancer Cell (2014) 26:754; Nature Comm (2014) 5:3446; EMBO J (2009) 28: 2220; Nature (2006) 442: 1058. Highly motivated individuals are encouraged to send CV and names of three references to:
Dr. X.F. Steven Zheng
University Professor and Co-Director, The Cancer Pharmacology Program, Rutgers Cancer Institute of New Jersey