Investigating cell-cell interactions in Drosophila glioma models
Logan J Roebke
Glioblastoma multiforme (GBM) is a devastating form of primary brain cancer with poor prognosis. Capitalizing on the similarities between mammalian and Drosophila glial cells, Drosophila glioblastoma models have been established that show similarities to anaplastic glia from high-grade human glioma. Using the Repo MARCM system, we established two models of Drosophila glioblastomas by overexpressing oncogene RasV12 together with downregulation of Pten (PtenRNAi) in one model system and suppression of scribble (ScribRNAi ) in another. These genetic alterations lead to overgrowth of glial cells creating glioblastomas in Drosophila larval brain. The glioblastoma containing brain appear enlarged in comparison to normal wild type brain, which clearly suggests the dysregulation of growth control in tumors. We studied expression of ecdysone receptor (ECR) and Taiman proteins in the two model glioblastomas. Taiman is the co-activator of ECR, and cooperatively control growth. One mechanism by which Taiman regulates growth is by cooperatively interacting with Yorkie (Yki) the co-activator of the Hippo growth control pathway. We want to understand the role of these proteins in the development of the gliomas. We first tested the expression of ECR and Taiman in our glioma models and found that in both the models, ECR and Taiman are downregulated in the tumor cells in comparison to the normal expression in non-tumor cells. This suggests the growth control is lost in tumors. We will test the role of Yki in this growth regulatory interaction. Here we present our findings from the ECR-Taiman-Yki studies in Drosophila glioma models.
Independent Research - Undergraduate
Primary Advisor's Department
Stander Symposium project
"Investigating cell-cell interactions in Drosophila glioma models" (2017). Stander Symposium Projects. 1059.