IndraLab

Statements


KCNH5 activates MB. 10 / 10
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"In this cancer, EAG-2 promotes the progression of the MB tumor by regulating cell volume dynamics, in turn inhibiting the tumor suppressor p38 MAPK pathway."

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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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"Moreover, EAG2 knockdown markedly reduced the motility of MB cells without affecting directionality, as did the EAG2 channel blocker astemizole, a known EAG2 channel blocker with an IC 50 of ~ 1.5 muM 32 (XREF_FIG)."

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"We demonstrate that pharmacological inhibition of EAG2 reduces MB cell viability and motility, and identify an FDA approved antipsychotic drug, thioridazine, as a novel EAG2 channel blocker with potent efficacy in reducing intracranial xenograft MB growth and metastasis."

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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."

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"EAG2 upregulation in metastatic MB of subsets of patients."

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"EAG2 knockdown not only impairs MB cell growth in vitro, but also reduces tumor burden in vivo and enhances survival in xenograft studies."

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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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"These results demonstrate that EAG2 promotes MB metastasis, a function distinct from its role in driving primary tumor growth."