ArticleMolecular neurobiology2019
An Adult Drosophila Glioma Model for Studying Pathometabolic Pathways of Gliomagenesis.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
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- Dual role of pseudogene TMEM198B in promoting lipid metabolism and immune escape of glioma cells.Oncogene · 2022Article
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- Modeling Brain Tumors: A Perspective Overview ofFrontiers in molecular neuroscience · 2022Review
- Cholesterol metabolism and its implication in glioblastoma therapy.Journal of Cancer · 2022Review
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- Modeling human brain tumors in flies, worms, and zebrafish: From proof of principle to novel therapeutic targets.Neuro-oncology · 2021Review
- Hypoxia-Induced miR-378a-3p Inhibits Osteosarcoma Invasion and Epithelial-to-Mesenchymal TransitionFrontiers in genetics · 2021Article
- Identification of glioblastoma-specific prognostic biomarkers via an integrative analysis of DNA methylation and gene expression.Oncology letters · 2020Article
- Strategies for Functional Interrogation of Big Cancer Data Using Drosophila Cancer Models.International journal of molecular sciences · 2020Review
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Glioblastoma multiforme (GBM), the most prevalent brain tumor in adults, has extremely poor prognosis. Frequent genetic alterations that activate epidermal growth factor receptor (EGFR) and phosphatidylinositol-3 kinase (PI3K) signaling, as well as metabolic remodeling, have been associated with gliomagenesis. To establish a whole-animal approach that can be used to readily identify individual pathometabolic signaling factors, we induced glioma formation in the adult Drosophila brain by activating the EGFR-PI3K pathway. Glioma-induced animals showed significantly enlarged brain volume, early locomotor abnormalities, memory deficits, and a shorter lifespan. Combining bioinformatics analysis and glial-specific gene knockdown in the adult fly glioma model, we identified four evolutionarily conserved metabolic genes, including ALDOA, ACAT1, ELOVL6, and LOX, that were involved in gliomagenesis. Silencing of ACAT1, which controls cholesterol homeostasis, reduced brain enlargement and increased the lifespan of the glioma-bearing flies. In GBM patients, ACAT1 is overexpressed and correlates with poor survival outcomes. Moreover, pharmacological inhibition of ACAT1 in human glioma cell lines revealed that it is essential for tumor proliferation. Collectively, these results imply that ACAT1 is a potential therapeutic target, and cholesterol homeostasis is strongly related to glioma formation. This in vivo model provides several rapid and robust phenotypic readouts, allowing determination of the pathometabolic pathways involved in gliomagenesis, as well as providing valuable information for novel therapeutic strategies.
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