IndraLab

Statements

KCNH5 activates Neoplasm Metastasis. 6 / 7
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reach
"Using multiple Drosophila brain tumor models induced by oncogene overexpression or loss of tumor suppressors to complement our study of mice with xenografted human MB cells, we show that the functions of EAG2 and Eag channel to promote malignant growth and metastasis are evolutionarily conserved (XREF_FIG)."
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"These results demonstrate that EAG2 promotes MB metastasis, a function distinct from its role in driving primary tumor growth."
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"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."
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"We find that EAG2 channel is enriched at the trailing edge of migrating MB cells to regulate local cell volume dynamics thereby facilitating cell motility, and EAG2 knockdown impairs MB metastasis in a xenograft model."
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"The finding of elevated EAG2 expression in metastatic lesions raised the prospect that EAG2 may promote MB metastasis or tumor growth at the disseminated site."
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"We identified 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."
26258683