Scholarlink

<p>This study investigates the anti-tumor mechanism of Cinobufagin (CBG) injection against gastric cancer. <i>In vivo</i>, CBG injection significantly suppressed xenograft tumor growth in nude mice. <i>In vitro</i>, it inhibited gastric cancer cell proliferation in a concentration-dependent manner and induced ferroptosis, evidenced by characteristic mitochondrial shrinkage, lipid reactive oxygen species accumulation, and an altered redox balance (e.g., elevated MDA, depleted GSH). To elucidate the underlying mechanism, we performed metabolomic profiling and Western blotting, which identified acyl-CoA synthetase long-chain family member 4 (ACSL4), a key regulator of lipid metabolism, as a critical target. CBG injection markedly upregulated ACSL4 expression. The functional relevance of ACSL4 was confirmed by rescue experiments: both pharmacological inhibition and genetic silencing of ACSL4 effectively reversed CBG injection-induced cell death and lipid peroxidation. In conclusion, CBG injection exerts its potent anti-gastric cancer effect by upregulating ACSL4. This upregulation drives lipid metabolic reprogramming, leading to lethal lipid peroxidation and subsequent ferroptosis. Our findings establish CBG injection as a promising therapeutic candidate for gastric cancer by targeting the ACSL4-dependent ferroptosis pathway.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Cinobufagin injection induces gastric cancer cell ferroptosis by regulating the ACSL4-mediated lipid peroxidation pathway

  • 期刊论文

  • 发表日期：

    2026年3月28日

查看全文
  • Yaping Ma,
  • Jing Chu,
  • Xiaxia Liu,
  • Jiao Long,
  • Zhangjie Wang,
  • Meng Wang,
  • Qinglin Li,
  • Huan Wu,
  • Hui Cheng

摘要

This study investigates the anti-tumor mechanism of Cinobufagin (CBG) injection against gastric cancer. In vivo, CBG injection significantly suppressed xenograft tumor growth in nude mice. In vitro, it inhibited gastric cancer cell proliferation in a concentration-dependent manner and induced ferroptosis, evidenced by characteristic mitochondrial shrinkage, lipid reactive oxygen species accumulation, and an altered redox balance (e.g., elevated MDA, depleted GSH). To elucidate the underlying mechanism, we performed metabolomic profiling and Western blotting, which identified acyl-CoA synthetase long-chain family member 4 (ACSL4), a key regulator of lipid metabolism, as a critical target. CBG injection markedly upregulated ACSL4 expression. The functional relevance of ACSL4 was confirmed by rescue experiments: both pharmacological inhibition and genetic silencing of ACSL4 effectively reversed CBG injection-induced cell death and lipid peroxidation. In conclusion, CBG injection exerts its potent anti-gastric cancer effect by upregulating ACSL4. This upregulation drives lipid metabolic reprogramming, leading to lethal lipid peroxidation and subsequent ferroptosis. Our findings establish CBG injection as a promising therapeutic candidate for gastric cancer by targeting the ACSL4-dependent ferroptosis pathway.