ArticleCancer cell international2025
Regulatory role of N-nitroso compounds and lncRNA NEAT1 in endoplasmic reticulum stress and malignant transformation of gastric epithelial cells.
Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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