Authors
Joos Berghausen, Emre Deniz, Ze-Jun Wang, Marcel Schmidt, Junfeng Ma, Karen Creswell, Aykut Üren, Eric Glasgow, Anton Wellstein, Tinatin I Brelidze
Published in
The Journal of biological chemistry. Pages 113590. Sep 22, 2026. Epub Sep 22, 2026.
Abstract
The voltage-gated potassium channel EAG1 is aberrantly expressed in many cancers, yet its mechanistic contributions to tumor growth and metastasis in non-small cell lung cancer (NSCLC) remains poorly defined. Here, we establish a genetic EAG1 knockout in A549 NSCLC cells and demonstrate that loss of EAG1 markedly suppresses tumor growth and metastasis using a combination of tissue culture, xenograft and multi-omics approaches. EAG1 knockout reduced proliferative ability across multiple in vitro assays and in vivo zebrafish xenografts. Furthermore, loss of EAG1 induced G1-phase cell-cycle arrest, accompanied by broad suppression of cell-cycle regulators. Additionally, knocking out EAG1 significantly reduced migratory and invasive properties in vitro, and markedly impaired extravasation in vivo. Integrated transcriptomic and proteomic analyses revealed that EAG1 regulates E2F signaling and epithelial-mesenchymal transition (EMT). Consistent with this, EAG1 knockout attenuated TGF-β-induced EMT by disrupting the cadherin switch, a key mechanism for EMT, and abolished EMT-driven migration, demonstrating that EAG1 is required for the acquisition of a migratory phenotype. Together, these findings establish EAG1 as a central regulator of proliferation and metastasis of A549 cells, highlighting EAG1 as a potential therapeutic target in NSCLC.
PMID:
42772558
Bibliographic data and abstract were imported from PubMed on 23 Sep 2026.
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