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EAG2 potassium channel with evolutionarily conserved function as a brain tumor target

ABSTRACT: Microarray profiling of amplified total RNA isolated from FACS-sorted Drosophila neuroblasts

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE70647 | GEO | 2015/08/09

SECONDARY ACCESSION(S): PRJNA289258

REPOSITORIES: GEO

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EAG2 potassium channel with evolutionarily conserved function as a brain tumor target

Project description:Microarray profiling of amplified total RNA isolated from FACS-sorted Drosophila neuroblasts 2 samples per group, RNA isolated and amplified. Hybridized as a one color experiment.

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EAG2 potassium channel with evolutionarily conserved function as a brain tumor target

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EAG2 potassium channel with evolutionarily conserved function as a brain tumor target

Project description:Characterizing the impact of pharmacological and shRNA-mediated silencing of EAG2 in medulloblastoma. Medulloblastoma (MB) is the most common pediatric CNS malignancy. Previously, we demonstrated that overexpression of the ion channel EAG2, identified in a subset of histological and molecular subtypes of this disease, functionally contributes to tumor progression (PMID: 22855790). Here, we demonstrate the evolutionarily conserved function of EAG2 potassium channel in promoting brain tumor growth and metastasis, delineate downstream pathways and uncover a co-option mechanism for different potassium channels to regulate mitotic cell volume and tumor progression. We show that EAG2 potassium channel is enriched at the trailing edge of migrating MB cells to regulate local cell volume dynamics, thereby facilitating cell motility. We identify the FDA- approved antipsychotic drug thioridazine as an EAG2 channel blocker that reduces xenografted MB growth and metastasis, and present a case report of repurposing thioridazine for treating a human patient. Our findings thus illustrate the potential of targeting ion channels in cancer treatment.

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