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Peer-reviewedCC BY 4.0The Journal of Biological Chemistry

EAG1 channel is a central regulator of tumor growth and metastasis in A549 non-small cell lung cancer cells

  • Joos Berghausen1
  • Emre Deniz2
  • Ze-Jun Wang1
  • Marcel Schmidt2
  • Junfeng Ma2
  • Karen Creswell2
  • Aykut Üren2
  • Eric Glasgow2
  • Anton Wellstein2
  • Tinatin I. Brelidze1
  1. 1Department of Pharmacology and Physiology, Georgetown University Medical Center, Washington, District of Columbia, USA
  2. 2Department of Oncology, Georgetown University Medical Center, Washington, District of Columbia, USA
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Abstract

The voltage-gated potassium channel Ether-à-go-go 1 (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 transforming growth factor-beta–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.

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Cite

BibTeXRIS
BibTeX
@article{berghausen2026eag1,
  title = {{EAG1 channel is a central regulator of tumor growth and metastasis in A549 non-small cell lung cancer cells}},
  author = {Joos Berghausen and Emre Deniz and Ze-Jun Wang and Marcel Schmidt and Junfeng Ma and Karen Creswell and Aykut Üren and Eric Glasgow and Anton Wellstein and Tinatin I. Brelidze},
  journal = {The Journal of Biological Chemistry},
  year = {2026},
  month = sep,
  doi = {10.1016/j.jbc.2026.113590},
  url = {https://doi.org/10.1016/j.jbc.2026.113590},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - EAG1 channel is a central regulator of tumor growth and metastasis in A549 non-small cell lung cancer cells
AU  - Joos Berghausen
AU  - Emre Deniz
AU  - Ze-Jun Wang
AU  - Marcel Schmidt
AU  - Junfeng Ma
AU  - Karen Creswell
AU  - Aykut Üren
AU  - Eric Glasgow
AU  - Anton Wellstein
AU  - Tinatin I. Brelidze
PY  - 2026
DA  - 2026/09/23
JO  - The Journal of Biological Chemistry
DO  - 10.1016/j.jbc.2026.113590
UR  - https://doi.org/10.1016/j.jbc.2026.113590
AB  - The voltage-gated potassium channel Ether-à-go-go 1 (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 transforming growth factor-beta–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.
SN  - 0021-9258
SN  - 1083-351X
ER  -