Area of Study
Science and Mathematics
Aberrant expression of members of the phosphatase of regenerating liver (PRL) family has been implicated as a key factor in the progression of several forms of human cancers. However, despite a wide range of studies supporting the role of the enzyme PRL as an oncogene, it has also been identified as a growth suppressor when tested under different conditions. One proposed explanation for this change in function is that redox regulation controls the accessibility of the active site of PRLs, which is necessary for oncogenic output. In this study, cellular redox environment was altered in vivo using Drosophila melanogaster, the common fruit fly, as a model organism. Enzymes promoting either reduction or oxidation were overexpressed alongside dPRL-1 in the eye and dorsal wing tissue, and analysis of the resulting phenotypes revealed that dPRL-1 suppresses growth in oxidized cells. When cells were reduced, as occurs in cancerous cells, dPRL-1 acted as either a stronger growth suppressor or a growth promoter depending on which reduction enzymes were altered. These results suggest that the impact of redox environment on PRL function is more complex than anticipated, and further research is necessary to fully understand the role of PRL in cancer development.
Welsh, Frances, "Effect of Altered Cellular Redox Environment on Oncogenic Activity of the Drosophila PRL Protein" (2015). Summer Research. 258.
University of Puget Sound