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<p>Astrocyte elevated gene-1 (AEG-1) is oncogenic in gastric cancer; however, its underlying mechanism has not been fully elucidated. In this study, we identified serine 308 (Ser308) as a phosphorylation site of AEG-1 in gastric cancer cells. By constructing AEG-1 point mutants to overexpress phospho-mimetic AEG-1 (S308D, serine-to-aspartate) and dephospho-mimetic AEG-1 (S308A, serine-to-alanine), we found that phosphorylation of AEG-1 at Ser308 significantly suppressed cell growth and migration, accompanied by downregulation of p65 NF-κB–mediated transcription of the downstream target genes <i>FOS</i> and <i>IL-8</i>. Mechanistically, TNF-α–induced dephosphorylation of AEG-1 at Ser308 promoted p65 NF-κB nuclear accumulation and activation through protein–protein interaction. This study reveals a novel phosphorylation-dependent switch that regulates AEG-1–mediated NF-κB signaling in gastric cancer.</p>

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Phosphorylation of AEG-1 suppresses NF-κB signaling in gastric cancer

  • 期刊论文

  • 发表日期：

    2026年5月26日

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  • Qihao Sun,
  • Zhihui Bai,
  • Jiajie Sun,
  • Tiantian Xiao,
  • Qingqing Zhang,
  • Xinyuxue Yang,
  • Xuerong Wang,
  • Zuhao Zhang,
  • Wenbin Huang

摘要

Astrocyte elevated gene-1 (AEG-1) is oncogenic in gastric cancer; however, its underlying mechanism has not been fully elucidated. In this study, we identified serine 308 (Ser308) as a phosphorylation site of AEG-1 in gastric cancer cells. By constructing AEG-1 point mutants to overexpress phospho-mimetic AEG-1 (S308D, serine-to-aspartate) and dephospho-mimetic AEG-1 (S308A, serine-to-alanine), we found that phosphorylation of AEG-1 at Ser308 significantly suppressed cell growth and migration, accompanied by downregulation of p65 NF-κB–mediated transcription of the downstream target genes FOS and IL-8. Mechanistically, TNF-α–induced dephosphorylation of AEG-1 at Ser308 promoted p65 NF-κB nuclear accumulation and activation through protein–protein interaction. This study reveals a novel phosphorylation-dependent switch that regulates AEG-1–mediated NF-κB signaling in gastric cancer.