Date of Award

5-9-2009

Degree Type

Thesis

Degree Name

Honors Thesis

Department

Pharmacy

Abstract

Prostate cancer is the second leading cause of cancer death in American men. The disease prognosis is significantly limited by the finite therapeutic treatments. The limited treatment options are made worse by the significant reduction in the quality of life that often results from the severe side effects produced by these treatments.1 Therefore, any improvements of current treatments would be advantageous to the clinical setting. Recently, TREK-1, a tandem-pore domain (K2P) potassium channel, has been shown to be upregulated in prostate cancer, but absent in normal prostate tissue.2 The observation that TREK-1 expression is correlated with tumor malignancy suggests that TREK-1 may be a possible target for the development of novel drugs that target prostate cancer. Interestingly, other subtypes of the K2P family also have upregulated expression in several other types of malignancies.2, 3, 4 These observations have prompted many research laboratories to characterize the role of TREK-1 in cancer cells. However, in order to explore the role of TREK-1 in cancer cells, pharmacological tools selective for TREK-1 need to be developed. Specifically, a large-scale screen is needed to identify molecules that selectively modulate TREK-1.