Associate Professor, Eppley Institute
Molecular mechanisms and therapeutic targets of metastasis
Summary of Research
Metastasis is the cause of 90 percent of deaths from cancer, and yet little is known about its underlying mechanisms. Therapies to treat metastatic disease are very limited. Traditional chemotherapy and radiotherapy are limited by their lack of specificity. Molecular targeting of oncogenic signaling molecules has the potential to be a more effective approach for cancer treatment than those presently available. However, it has so far had a very limited clinical impact. Thus, there remains a need for the identification of potential cancer targets and development of novel target-specific therapies for cancer treatment. Understanding the mechanisms of metastasis will provide the new information necessary for drug development.
Metastatic cells acquire abnormal characteristics that facilitate their deadly behavior, including the ability to:
- invade tissue;
- induce angiogenesis, which allows cells to escape the limits that diffusion of nutrients and oxygen impose on tumor growth;
- survive in the circulation and in various foreign microenvironments before they colonize a target organ; and
- survive and proliferate within the stroma of the target organ.
The research in my lab focuses on understanding the molecular mechanisms of cancer metastasis and identification and validation of novel targets associated with cell survival, invasion, angiogenesis and metastasis such as gain-of-function mutation of Phosphatidylinositol 3-Kinase (PI3K), receptor tyrosine kinase Ron and Phosphatase of Regenerating Liver-3 (PRL-3). The ongoing research projects include:
- Identify and validate new targets associated with different characteristics of metastasis;
- Investigate the role of microRNAs, a special category of oncogenes or tumor suppressors, in cancer metastasis (using human cancer cells and in vivo mouse models) as well as their regulation by different signaling pathways;
- Investigate the role of cancer stem cells (or tumor initiating cells) in cancer metastasis and drug resistance.
Tel: 402-559-5558 (Office)
E-mail: Jenny Wang