Date of Award
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.
Surber, Susan Abigal, "Developing an Assay to Profile Upregulated TREK-1, A Stretch-Activated Potassium Channel, in Prostate Cancer" (2009). Undergraduate Honors Thesis Collection. Paper 67.