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<p>Ferroptosis is a novel form of cell death characterized by iron-dependent oxidative damage, lipid peroxidation, and the accumulation of reactive oxygen species. There exists a close correlation between ferroptosis and gastric cancer (GC). Recent research has shown that many ferroptosis-related long non-coding RNAs (lncRNAs) affect the occurrence and progression of GC. However, the exact mechanism has not been elucidated. This study showed that a novel lncRNA LINC02266 was upregulated in GC cells and was a key lncRNA associated with GC prognosis and progression. Functional analysis indicated that LINC02266 suppressed ferroptosis and promoted GC cell proliferation, migration, invasion, and tumor growth in vitro and vivo. Mechanistically, we found that LINC02266 inhibited erastin-induced ferroptosis by suppressing ACSL4 levels, which may be related to the AKT pathway. This study indicates that LINC02266 can serve as a diagnostic marker and novel therapeutic target for GC.</p>

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LINC02266 promotes proliferation and metastasis and inhibits ferroptosis of gastric cancer cells by regulating AKT/ACSL4 pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月19日

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  • Xiaoru Liang,
  • Xinyu Niu,
  • Lijie Zhang,
  • Chang Liu,
  • Xiaomin Zhao,
  • Feng Chen,
  • Zhijuan Lin

摘要

Ferroptosis is a novel form of cell death characterized by iron-dependent oxidative damage, lipid peroxidation, and the accumulation of reactive oxygen species. There exists a close correlation between ferroptosis and gastric cancer (GC). Recent research has shown that many ferroptosis-related long non-coding RNAs (lncRNAs) affect the occurrence and progression of GC. However, the exact mechanism has not been elucidated. This study showed that a novel lncRNA LINC02266 was upregulated in GC cells and was a key lncRNA associated with GC prognosis and progression. Functional analysis indicated that LINC02266 suppressed ferroptosis and promoted GC cell proliferation, migration, invasion, and tumor growth in vitro and vivo. Mechanistically, we found that LINC02266 inhibited erastin-induced ferroptosis by suppressing ACSL4 levels, which may be related to the AKT pathway. This study indicates that LINC02266 can serve as a diagnostic marker and novel therapeutic target for GC.