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Glioblastoma is the most common form of malignant brain tumor with a poor prognosis. Using a Drosophila glioma model, we showed that the Drosophila Tep1 gene (human CD109) regulates Yki (human YAP/TAZ) via an evolutionarily conserved mechanism. Oncogenic signaling by the YAP/TAZ pathway occurs in cells that acquire CD109 expression. Loss of Tep1 caused a reduction in glioma growth. Further, Tep1 affects Yki mediated stem cell renewal in glioma, as reduction of Tep significantly decreases the number of neuroblasts in glioma. Thus, we identify Tep1-Yki interaction in the larval CNS that plays a key role in glioma growth and progression.
Gangwani, Karishma, "Tep1 Regulates Yki Activity in Neural Stem Cells in Drosophila Glioma Model" (2021). Graduate Student Showcase. 3.