Pro-tumoral Ca signaling is dependent on Slowpoke and Ca-α1T channels in Drosophila melanogaster glioma
Ion channel-mediated cytosolic Ca oscillations play a crucial role in promoting glioblastoma growth. Here, we have studied the expression and functional roles of prospective oncogenic targets Slowpoke and Ca-α1T channels in a Drosophila melanogaster glioma model. While their mammalian orthologs have...
| Autores: | , , , , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2026 |
| País: | España |
| Institución: | Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya) |
| Repositorio: | Recercat. Dipósit de la Recerca de Catalunya |
| OAI Identifier: | oai:dnet:recercat____::37d2568f3d1ef55bcf9bd1e059d3d546 |
| Acceso en línea: | https://doi.org/10.1038/s41598-026-42712-8 https://hdl.handle.net/10459.1/470065 |
| Access Level: | acceso abierto |
| Palabra clave: | Calcium Glioma Ion channels Oncogenic pathways Proliferation |
| Sumario: | Ion channel-mediated cytosolic Ca oscillations play a crucial role in promoting glioblastoma growth. Here, we have studied the expression and functional roles of prospective oncogenic targets Slowpoke and Ca-α1T channels in a Drosophila melanogaster glioma model. While their mammalian orthologs have shown to be relevant for glioblastoma cell viability in vitro, there is no data available about their oncogenic function in a complex in vivo environment. Using RNAis against Slowpoke and Ca-α1T specifically expressed in glial cells, we show that both channels contribute to magnify Ca activity and ensuing Ca-dependent pro-tumoral pathways, glial cell proliferation and membrane extension. However, only the knockdown of Slowpoke extends the lifespan of glioma-bearing individuals and reverses glioma-induced neurodegeneration, suggesting its functional association with other Ca channels in addition to Ca-α1T. Furthermore, RNAseq transcriptomic analysis reveals that Slowpoke regulates excitatory neurotransmission, highlighting its potential as a therapeutic target in glioblastoma. |
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