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<p>Ion channel-mediated cytosolic Ca<sup>2+</sup> 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 <i>Drosophila melanogaster</i> 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 <i>Slowpoke</i> and <i>Ca-α1T</i> specifically expressed in glial cells, we show that both channels contribute to magnify Ca<sup>2+</sup> activity and ensuing Ca<sup>2+</sup>-dependent pro-tumoral pathways, glial cell proliferation and membrane extension. However, only the knockdown of <i>Slowpoke</i> extends the lifespan of glioma-bearing individuals and reverses glioma-induced neurodegeneration, suggesting its functional association with other Ca<sup>2+</sup> channels in addition to Ca-α1T. Furthermore, RNAseq transcriptomic analysis reveals that <i>Slowpoke</i> regulates excitatory neurotransmission, highlighting its potential as a therapeutic target in glioblastoma.</p>

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Pro-tumoral Ca2+ signaling is dependent on Slowpoke and Ca-α1T channels in Drosophila melanogaster glioma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月6日

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  • Lía Alza,
  • Patricia Montes-Labrador,
  • Diego Megías,
  • Andreu Casali,
  • Sergio Casas-Tintó,
  • Judit Herreros,
  • Carles Cantí

摘要

Ion channel-mediated cytosolic Ca2+ 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 Ca2+ activity and ensuing Ca2+-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 Ca2+ 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.