Recent evidence has proved that curcumin as a natural polyphenol have a great anticancer and anti‐proliferative effects in cancer cells. Ferroptosis, a new form of regulated cell death, plays a vital role in the pathogenesis and therapy of cancers. In this study, we aimed to examine the effects of curcumin in ferroptosis of human colorectal cancer cells and its underlying molecular mechanisms. SW‐480 colorectal cancer cells were treated by curcumin with different concentrations. Cell viability was determined by using MTT assay. The concentrations of reactive oxygen species (ROS) and intracellular iron were measured using specific related kits. Real‐time PCR and Western blot analysis were used to determine the expression of ferroptosis‐related proteins including ACSL4, GPx4 and FTH1 and activation of JNK protein. Curcumin suppressed SW‐480 cancer cells viability in dose‐dependent manner. Cell treatment with curcumin led to accumulation of ROS and iron within cells and increase in the intracellular levels of lipid peroxidation. In addition, curcumin modulated the mRNA and protein expression levels of ferroptosis‐related proteins including ACSL4, GPx4 and FTH1 and suppression of JNK signaling. Curcumin may exhibit its anticancer effect on colorectal cancer by downregulating JNK signaling to induce ferroptosis in SW‐480 cells.

中文翻译：

---

姜黄素激活JNK信号通路促进结肠癌细胞铁死亡

最近的证据证明，姜黄素作为一种天然多酚，具有很强的抗癌和抗癌细胞增殖作用。铁死亡是一种新的受调节细胞死亡形式，在癌症的发病机制和治疗中发挥着至关重要的作用。在这项研究中，我们旨在研究姜黄素对人结直肠癌细胞铁死亡的影响及其潜在的分子机制。用不同浓度的姜黄素处理SW-480结直肠癌细胞。通过使用MTT测定法测定细胞活力。使用特定的相关试剂盒测量活性氧（ROS）和细胞内铁的浓度。采用实时PCR和Western blot分析检测铁死亡相关蛋白ACSL4、GPx4和FTH1的表达以及JNK蛋白的激活。姜黄素以剂量依赖性方式抑制 SW-480 癌细胞的活力。用姜黄素处理细胞会导致细胞内活性氧和铁的积累，并增加细胞内脂质过氧化水平。此外，姜黄素还能调节铁死亡相关蛋白（包括 ACSL4、GPx4 和 FTH1）的 mRNA 和蛋白表达水平，并抑制 JNK 信号传导。姜黄素可能通过下调 JNK 信号传导诱导 SW-480 细胞铁死亡来发挥其对结直肠癌的抗癌作用。