As an innovative treatment strategy for cancer treatment, Fenton reaction-mediated chemodynamic therapy (CDT) dependent on the conversion of endogenous hydrogen peroxide (H₂O₂) into cytotoxic hydroxyl radical (•OH) to destroy tumor cells has attracted increasing interest. However, the insufficient supply of H₂O₂ has greatly hindered the anticancer efficacy of CDT in the tumor microenvironment, and this inherent disadvantage has rarely attracted attention. In order to develop a strategy with high-efficiency H₂O₂ self-supply ability to enhance the CDT efficacy, we constructed a Fe-based metal-organic framework (MOF) as a carrier for the drug Juglone (JUG), which can not only increase the intracellular H₂O₂ concentration, but also serve as an inhibitor of the peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1), which is a key regulator for multiple physiological processes in cancer cells. Once internalized by tumor cells, the acidic environment of the tumor promotes the release of JUG for drug therapy, and the released Fe ions trigger the Fenton reaction to produce •OH from sufficient H₂O₂, thereby achieving significant antitumor effects. Furthermore, the coating of cancer cell membranes onto the JUG-loaded MOF could enable it with homologous tumor targeting ability. Both in vitro and in vivo results show that the use of drugs can activate the cascade to provide sufficient H₂O₂ with outstanding anti-tumor efficacy, which paves a new avenue for the realization of drug/CDT synergistic therapy.

作为癌症治疗的一种创新治疗策略，芬顿反应介导的化学动力学疗法 (CDT) 依赖于内源性过氧化氢 (H ₂ O ₂ ) 转化为细胞毒性羟基自由基 (•OH) 来破坏肿瘤细胞，这引起了越来越多的关注。然而，H ₂ O _{2 的}供给不足，极大地阻碍了CDT在肿瘤微环境中的抗癌功效，而这一固有的劣势鲜少引起人们的关注。为了制定高效的 H ₂ O _{2 策略}为了提高CDT功效，我们构建了铁基金属有机骨架（MOF）作为药物胡桃酮（JUG）的载体，不仅可以增加细胞内H ₂ O ₂浓度，还可以作为作为肽基-脯氨酰基的抑制剂顺-反异构酶NIMA相互作用1（1脚），其是用于在癌细胞中的多个生理过程的关键调节剂。一旦被肿瘤细胞内化，肿瘤的酸性环境促进JUG释放用于药物治疗，释放的Fe离子引发芬顿反应，从足够的H ₂ O _{2 中}产生•OH，从而达到显着的抗肿瘤作用。此外，将癌细胞膜涂覆到负载 JUG 的 MOF 上可以使其具有同源的肿瘤靶向能力。二者在体外和体内结果显示，使用药物可以激活级联，以提供足够ħ ₂ ö ₂以优异的抗肿瘤功效，其铺平为实现药物/ CDT协同治疗的新途径。