Kathryn Lawson, Ph.D.

My laboratory uses genetically-modified human cell lines to study the way changes in cell adhesion proteins can contribute to tumor development. We are specifically interested in the role of P-cadherin, a molecule located on the sides of cells that helps hold cells together to form tissues, and N-cadherin, which becomes abnormally expressed in epithelial cancers. Current research efforts are focused on three areas in which cadherin expression may alter tumor development:


1. P-cadherin-dependent tumor progression in non-small cell lung cancer. Clinical studies have suggested that P-cadherin decreases overall survival in patients with non-small cell lung cancer tumors that have abnormally high levels of P-cadherin expression. We are using genetically-modified lung cancer cell lines to examine the mechanisms by which P-cadherin may promote tumor development and aggressiveness.

2. P-cadherin-dependent chemoresistance in Oral Squamous Cell Carcinoma. We have found that increased levels of P-cadherin can cause oral cells to exhibit either greater resistance or greater sensitivity to different classes of chemotheraputic drugs that are used to treat oral cancer. We are currently using a proteomics (protein-based) approach to define the P-cadherin-driven signaling networks that play an important role in cell death vs. cell survival in cells treated with these agents.

3. Metabolic consequences of N-cadherin in oral squamous cell carcinoma. We are using both an oral precancer and oral squamous carcinoma model system to evaluate the effects of N-cadherin on metabolic signaling, including stimulation the Warburg effect to increase both glucose utilization and anaerobic glycolysis.