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<p>This study investigates the anticancer effects of rosmarinic acid (RA) on colorectal cancer and elucidates its underlying mechanisms. A range of in vitro assays—including CCK-8, EdU incorporation, colony formation, wound healing, and Transwell invasion—demonstrated that RA significantly inhibited the proliferation, migration, and invasion of HCT-116 cells. Ferroptosis induction was confirmed by increased intracellular Fe<sup>2+</sup>, ROS, and MDA levels, decreased glutathione, and characteristic mitochondrial damage observed via transmission electron microscopy. Bioinformatics analysis and molecular docking identified key ferroptosis-related targets of RA, particularly AKR1C3 and PTGS2, which are involved in arachidonic acid metabolism and inflammation. RT-qPCR and Western blot assays validated that RA downregulates PTGS2 while upregulating AKR1C3, ACSL4, and LPCAT3, indicating that RA may promote ferroptosis through metabolic reprogramming and oxidative injury. These findings suggest that RA exerts its anticancer activity by triggering ferroptosis via mitochondrial dysfunction and modulation of lipid metabolic pathways. This study provides novel insight into the molecular mechanism of RA and highlights its therapeutic potential as a ferroptosis inducer for colorectal cancer treatment.</p>

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Rosmarinic acid induces ferroptosis in colon cancer: insights from AKR1C3/PTGS2 pathway and mitochondrial dysfunction

  • 期刊论文

  • 发表日期：

    2025年10月6日

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  • Jincheng Tang,
  • Jingting Zhang,
  • Hongyao Chen,
  • Zhibin Wang,
  • Ling Wu,
  • Peisen Xue,
  • Renyi Yang,
  • Wei Peng,
  • Puhua Zeng

摘要

This study investigates the anticancer effects of rosmarinic acid (RA) on colorectal cancer and elucidates its underlying mechanisms. A range of in vitro assays—including CCK-8, EdU incorporation, colony formation, wound healing, and Transwell invasion—demonstrated that RA significantly inhibited the proliferation, migration, and invasion of HCT-116 cells. Ferroptosis induction was confirmed by increased intracellular Fe2+, ROS, and MDA levels, decreased glutathione, and characteristic mitochondrial damage observed via transmission electron microscopy. Bioinformatics analysis and molecular docking identified key ferroptosis-related targets of RA, particularly AKR1C3 and PTGS2, which are involved in arachidonic acid metabolism and inflammation. RT-qPCR and Western blot assays validated that RA downregulates PTGS2 while upregulating AKR1C3, ACSL4, and LPCAT3, indicating that RA may promote ferroptosis through metabolic reprogramming and oxidative injury. These findings suggest that RA exerts its anticancer activity by triggering ferroptosis via mitochondrial dysfunction and modulation of lipid metabolic pathways. This study provides novel insight into the molecular mechanism of RA and highlights its therapeutic potential as a ferroptosis inducer for colorectal cancer treatment.