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Background <p>The progression of esophageal cancer (EC) has been associated with aberrant activation of oncogenes and suppression of tumor suppressor genes. The EZR gene encodes ezrin, which is highly activated and upregulated in cancer cells, contributing to their invasive potential. This study aimed to elucidate the role of ezrin in EC progression, with a specific focus on the PI3K-AKT signaling pathway.</p> Method <p>Expression of the <i>EZR</i> gene was silenced in ECA109 cells to assess changes in the phosphorylation levels of multiple kinases Bioinformatics analyses were conducted to identify ezrin-associated signaling pathways. In vitro functional assays were performed to investigate the effects of <i>EZR</i> silencing on cell proliferation, apoptosis, migration, and invasion.</p> Results <p>Cells with <i>EZR</i> knockdown demonstrated markedly decreased phosphorylation of AKT1/2/3 (S473), EGFR (Y1086), PLC-γ1 (Y783), Src (Y419), STAT5a/b (Y694/Y699), Yes (Y426), and β-Catenin, relative to control cells. These findings indicate that the PI3K-AKT signaling pathway is a critical downstream mediator of ezrin activity. The inhibition of AKT phosphorylation resulting from <i>EZR</i> knockdown was reversed upon treatment with an AKT pathway activator, confirming the involvement of this signaling axis. Functionally, <i>EZR</i> silencing significantly reduced EC cell proliferation, migration, and invasion, and increased apoptosis. These effects were attenuated, in part, by concurrent activation of the AKT pathway. Collectively, the data suggest that ezrin modulates key oncogenic processes in EC through the PI3K-AKT signaling pathway.</p> Conclusion <p>Ezrin contributes to the progression of EC through modulation of the PI3K-AKT signaling cascade, influencing cellular proliferation, apoptosis, migration, and invasion.</p>

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Regulatory role of ezrin in esophageal cancer progression via the PI3K-AKT signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月30日

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  • Yuefeng Zhang,
  • Qifeng Zhao,
  • Jie Du

摘要

Background

The progression of esophageal cancer (EC) has been associated with aberrant activation of oncogenes and suppression of tumor suppressor genes. The EZR gene encodes ezrin, which is highly activated and upregulated in cancer cells, contributing to their invasive potential. This study aimed to elucidate the role of ezrin in EC progression, with a specific focus on the PI3K-AKT signaling pathway.

Method

Expression of the EZR gene was silenced in ECA109 cells to assess changes in the phosphorylation levels of multiple kinases Bioinformatics analyses were conducted to identify ezrin-associated signaling pathways. In vitro functional assays were performed to investigate the effects of EZR silencing on cell proliferation, apoptosis, migration, and invasion.

Results

Cells with EZR knockdown demonstrated markedly decreased phosphorylation of AKT1/2/3 (S473), EGFR (Y1086), PLC-γ1 (Y783), Src (Y419), STAT5a/b (Y694/Y699), Yes (Y426), and β-Catenin, relative to control cells. These findings indicate that the PI3K-AKT signaling pathway is a critical downstream mediator of ezrin activity. The inhibition of AKT phosphorylation resulting from EZR knockdown was reversed upon treatment with an AKT pathway activator, confirming the involvement of this signaling axis. Functionally, EZR silencing significantly reduced EC cell proliferation, migration, and invasion, and increased apoptosis. These effects were attenuated, in part, by concurrent activation of the AKT pathway. Collectively, the data suggest that ezrin modulates key oncogenic processes in EC through the PI3K-AKT signaling pathway.

Conclusion

Ezrin contributes to the progression of EC through modulation of the PI3K-AKT signaling cascade, influencing cellular proliferation, apoptosis, migration, and invasion.