Tep1 Regulates Yki Activity in Neural Stem Cells in Drosophila Glioma Model.

摘要: Glioblastoma Multiforme (GBM) is the most common form of malignant brain tumor with poor prognosis. Amplification Epidermal Growth Factor Receptor (EGFR), and mutations leading to activation Phosphatidyl-Inositol-3 Kinase (PI3K) pathway are commonly associated GBM. Using a previously published Drosophila glioma model generated by coactivation PI3K EGFR pathways [by downregulation Pten overexpression oncogenic Ras] in glial cells, we showed that Tep1 gene (ortholog human CD109) regulates Yki (the ortholog YAP/TAZ) via an evolutionarily conserved mechanism. Oncogenic signaling YAP/TAZ occurs cells acquire CD109 expression response inflammatory environment induced radiation clinically relevant models. Further, caused reduction activity reduced growth. A key function larval CNS stem cell renewal formation neuroblasts. Other reports suggest different upstream regulators optic lobe versus central regions CNS. We hypothesized interacts Hippo effector regulate neuroblast numbers. tested if acts through affect growth, normal affects number proliferation. Our data suggests mediated glioma, as Tep significantly decreases neuroblasts glioma. Thus, identify Tep1-Yki interaction plays role growth progression.