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• W3044142629 abstract "Abstract Glioblastoma (GBM), a very aggressive and incurable tumor, often results from constitutive activation of EGFR (epidermal growth factor receptor) and of PI3K (phosphoinositide 3-kinase). To understand the role of autophagy in the pathogenesis of glial tumors in vivo , we used an established Drosophila melanogaster model of glioma based on overexpression in larval glial cells of an active human EGFR and of the PI3K homolog Dp110 . Interestingly, the resulting hyperplastic glia expresses high levels of ref(2)P (refractory to Sigma P), the Drosophila homolog of p62/SQSTM1. However, cellular clearance of autophagic cargoes appears inhibited upstream of autophagosome formation. Remarkably, downregulation of subunits of the vacuolar-H+-ATPase (V-ATPase) prevents overgrowth, reduces PI3K signaling and restores clearance. Consistent with evidence in flies, neurospheres from patients with high V-ATPase subunit expression show inhibition of autophagy. Altogether, our data suggest that autophagy is repressed during glial tumorigenesis and that V-ATPase could represent a therapeutic target against GBM." @default.
• W3044142629 created "2020-07-29" @default.
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• W3044142629 date "2020-07-21" @default.
• W3044142629 modified "2023-09-25" @default.
• W3044142629 title "V-ATPase controls tumor growth and autophagy in aDrosophilamodel of gliomagenesis" @default.
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• W3044142629 doi "https://doi.org/10.1101/2020.07.20.211565" @default.
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