氯化血红素可触发细胞内活性氧 (ROS) 积累并增强血红素加氧酶-1 (HOX-1) 活性，表明其作为抗癌剂的潜力，尽管精确控制其细胞内水平至关重要。该研究探讨了氯化血红素及其衍生物、氯化血红素-酪氨酸和氯化血红素-苯乙烯 (H-Styr) 缀合物对乳腺癌细胞迁移、HOX-1 表达、特异性凋亡标记物、线粒体功能和 ROS 生成的影响。使用分子对接和动力学模拟来了解 HOX-1、血红素和化合物之间的相互作用。血红素在诱导 HOX-1 表达、表现出促氧化作用和减少细胞迁移方面优于其衍生物。分子模拟表明，血红素主要通过范德华力和静电力与 HOX-1 有利结合，其次是其他化合物。然而，只有范德华力决定 H-Styr 络合。这些相互作用受金属卟啉特性的影响，为 HOX-1 调节和 ROS 生成提供了见解，有可能指导针对氧化应激的乳腺癌疗法的开发。

Hemin triggers intracellular reactive oxygen species (ROS) accumulation and enhances heme oxygenase-1 (HOX-1) activity, indicating its potential as an anticancer agent, though precise control of its intracellular levels is crucial. The study explores the impact of hemin and its derivatives, hemin-tyrosine, and hemin-styrene (H-Styr) conjugates on migration, HOX-1 expression, specific apoptosis markers, mitochondrial functions, and ROS generation in breast cancer cells. Molecular docking and dynamics simulations were used to understand the interactions among HOX-1, heme, and the compounds. Hemin outperforms its derivatives in inducing HOX-1 expression, exhibiting pro-oxidative effects and reducing cell migration. Molecular simulations show that heme binds favorably to HOX-1, followed by the other compounds, primarily through van der Waals and electrostatic forces. However, only van der Waals forces determine the H-Styr complexation. These interactions, influenced by metalloporphyrin characteristics, provide insights into HOX-1 regulation and ROS generation, potentially guiding the development of breast cancer therapies targeting oxidative stress.