Understanding how the loss of Dronc function affects apoptosis
Cancer is caused by mutations in cells that disrupt signals for growth and division. Apoptosis, a system of programmed cell death, is controlled by genes and impacts cell survival, proliferation, and differentiation. Dysregulation of apoptosis is a significant cause of cancer, as mutated tumor cells show uncontrolled growth and elude cell death. Because of this, it is crucial to study how the genes involved in cell growth and death pathways become dysregulated in a way that causes tumor creation, so that cancer biology can be better understood and possible therapeutic measures can be pursued. One pathway commonly dysregulated in human tumors, the Hippo pathway, was identified in Drosophila melanogaster and is conserved evolutionarily in humans. Former research in our lab has shown that the Hippo pathway interacts with initiator caspase Dronc, which is the first target gene to be negatively regulated by this pathway, in the regulation of apoptosis. We hypothesize that loss of Dronc function would enable unchecked cell proliferation. To assess this, we are using RNAi to interfere with Dronc expression. We will also use markers like cyclin A, B, and E to evaluate cell proliferation through immunostaining and confocal microscopy. Here we present our findings on the how the loss of Dronc affects cell proliferation.
Primary Advisor's Department
Stander Symposium poster
"Understanding how the loss of Dronc function affects apoptosis" (2018). Stander Symposium Posters. 1316.