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<p>This study investigates the early oncogenic transformation of gastric epithelial cells (GES-1) and adenocarcinoma cells (AGS) following long-term exposure to N-nitroso compounds (NOCs), using N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) as a model carcinogen. Prolonged MNNG treatment enhanced proliferation, migration, invasion, and anchorage-independent growth. These effects were accompanied by persistent activation of endoplasmic reticulum stress (ERS) and autophagy, characterized by elevated PERK, eIF2α, ATF4, CHOP, Beclin-1, and LC3-II, and reduced p62. Long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) was markedly upregulated and acted as a competing endogenous RNA, sponging microRNA-329-3p (miR-329-3p) to derepress ATF4. Silencing NEAT1 or restoring miR-329-3p expression suppressed ERS, autophagy, and malignant traits. These findings establish a NEAT1/miR-329-3p/ATF4 signaling axis that links stress response to early gastric epithelial transformation, offering a potential target for intervention.</p>

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Regulatory role of N-nitroso compounds and lncRNA NEAT1 in endoplasmic reticulum stress and malignant transformation of gastric epithelial cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月3日

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  • Xing Liu,
  • Yichun Zhao,
  • Yueyue Zhou,
  • Xihuan Zou,
  • Ruobing Chen,
  • Yuting Peng,
  • Meng Yu

摘要

This study investigates the early oncogenic transformation of gastric epithelial cells (GES-1) and adenocarcinoma cells (AGS) following long-term exposure to N-nitroso compounds (NOCs), using N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) as a model carcinogen. Prolonged MNNG treatment enhanced proliferation, migration, invasion, and anchorage-independent growth. These effects were accompanied by persistent activation of endoplasmic reticulum stress (ERS) and autophagy, characterized by elevated PERK, eIF2α, ATF4, CHOP, Beclin-1, and LC3-II, and reduced p62. Long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) was markedly upregulated and acted as a competing endogenous RNA, sponging microRNA-329-3p (miR-329-3p) to derepress ATF4. Silencing NEAT1 or restoring miR-329-3p expression suppressed ERS, autophagy, and malignant traits. These findings establish a NEAT1/miR-329-3p/ATF4 signaling axis that links stress response to early gastric epithelial transformation, offering a potential target for intervention.