ArticleCancer gene therapy2026
Amitriptyline inhibits EAG1 channels by binding to their PAS domains and exerts EAG1-dependent anti-tumorigenic effects.
Article in Cancer gene therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Potassium channels in cancer: from hallmarks to therapeutic targeting.Journal of physiology and biochemistry · 2026Review
- Repurposing tricyclic drugs as cancer therapeutics: comparative analysis of antitumorigenic effects of chlorpromazine, amitriptyline and imipramine.Frontiers in oncology · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
Ether-a-go-go 1 (EAG1) potassium channels are overexpressed in the majority of cancers, and inhibition of their activity decreases cancer growth and migration. Here, we show that amitriptyline (AmiT), an antidepressant that is also used for pain management in cancer patients, inhibits EAG1 by binding to their PAS domains and exerts EAG1-dependent anti-tumorigenic effects. AmiT inhibited the growth of MDA-MB-231 and SH-SY5Y cells expressing EAG1 at high levels, while having a smaller effect on the growth of A375 cells expressing EAG1 at lower levels. Knocking in EAG1 in HEK293 cells increased the inhibition of cell growth by AmiT, while knocking out EAG1 in MDA-MB-231 cells decreased the inhibition of cell growth by the drug. AmiT also inhibited cell migration in MDA-MB-231 and SH-SY5Y cells, while having no effect in A375 cells. Knocking out EAG1 in MDA-MB-231 cells completely removed the effect of AmiT on cell migration. Similar to the in vitro results, AmiT inhibited the growth of MDA-MB-231 and SH-SY5Y zebrafish xenografts, while having no effect on A375 xenografts. Taken together, these results indicate that EAG1 channels are a functional target of AmiT and suggest a potential repurposing of this FDA-approved drug as an anti-cancer agent for tumors with high EAG1 expression.
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