Brittany Allen-Petersen, PhD

Lung cancer is the leading cause of cancer-related deaths in the United States with only 25% of patients surviving for five years after diagnosis. Metastasis, or colonization of lung cancer cells in distant parts of the body, significantly contributes to this low survival rate. It represents an important clinical challenge as there are limited treatment options for these patients. For lung cancer cells to become metastatic, they lose their typical cell characteristics and start to gain more invasive properties in a process called epithelial-to-mesenchymal transition (EMT). Our research focuses on how protein phosphatases suppress the ability of lung cancer cells to undergo EMT. Protein phosphatases function as critical "off" switches in the cell and are commonly disrupted in cancer. We will investigate how a particular protein phosphatase, PP2A, regulates EMT and prevents resistance to therapies, increasing our understanding of this deadly disease.

Supported by the Mary Fuller Russell Fund

Update: The Allen-Petersen lab aims to understand how protein phosphatases function to suppress non-small cell lung cancer (NSCLC) progression and therapeutic response. Phosphatases function as off-switches to an enzyme called kinase, which sends signals inside cells to control the cell’s behavior. This function provides a critical regulation of pathways such as the NSCLC driver, the epidermal growth factor receptor (EGFR). We have determined that suppression of Protein Phosphatase 2A (PP2A) results in an epithelial to mesenchymal transition (EMT), a process that underlies metastatic tumor growth. As the tumor metastasizes, or changes, it undergoes major changes in the proteins produced. These changes affect how genes are controlled and can make thecancer less responsive to treatment. Patients whose tumors undergo these changes tend to have shorter survival. Our studies highlight phosphatases as novel regulators of NSCLC metastasis and indicate that PP2A may be a potential therapeutic target to weaken the progression of aggressive NSCLC.