卵巢癌（OC）是妇科恶性肿瘤中死亡率最高的，需要探索新颖、高效、低毒的治疗策略。铁死亡是一种由铁依赖性脂质过氧化诱导的程序性细胞死亡，可能会激活抗肿瘤免疫。开发高效的铁死亡诱导剂可以改善 OC 预后。在这项研究中，我们开发了一种超声可控二维 (2D) 压电纳米激动剂 (Bi2MoO6-MXene) 来诱导铁死亡。 Bi2MoO6 (BMO) 和 MXene 之间的肖特基异质结将带隙宽度减少了 0.44 eV，提高了载流子分离效率，并降低了超声刺激下电子-空穴对的复合率。因此，活性氧产率提高。在时空超声激励下，BMO-MXene有效抑制OC增殖90%以上，诱导脂质过氧化，降低线粒体膜电位，并使谷胱甘肽过氧化物酶和胱硫醚转运蛋白系统失活，从而引起肿瘤细胞铁死亡。 OC细胞中的铁死亡进一步激活免疫原性细胞死亡，促进树突状细胞成熟并刺激抗肿瘤免疫。我们成功开发了一种高效的铁死亡诱导剂（BMO-MXene），能够通过声动力-铁死亡-免疫原性细胞死亡途径抑制OC进展.© 2024。作者。

Ovarian cancer (OC) has the highest fatality rate among all gynecological malignancies, necessitating the exploration of novel, efficient, and low-toxicity therapeutic strategies. Ferroptosis is a type of programmed cell death induced by iron-dependent lipid peroxidation and can potentially activate antitumor immunity. Developing highly effective ferroptosis inducers may improve OC prognosis.In this study, we developed an ultrasonically controllable two-dimensional (2D) piezoelectric nanoagonist (Bi2MoO6-MXene) to induce ferroptosis. A Schottky heterojunction between Bi2MoO6 (BMO) and MXene reduced the bandgap width by 0.44 eV, increased the carrier-separation efficiency, and decreased the recombination rate of electron-hole pairs under ultrasound stimulation. Therefore, the reactive oxygen species yield was enhanced. Under spatiotemporal ultrasound excitation, BMO-MXene effectively inhibited OC proliferation by more than 90%, induced lipid peroxidation, decreased mitochondrial-membrane potential, and inactivated the glutathione peroxidase and cystathionine transporter protein system, thereby causing ferroptosis in tumor cells. Ferroptosis in OC cells further activated immunogenic cell death, facilitating dendritic cell maturation and stimulating antitumor immunity.We have succeeded in developing a highly potent ferroptosis inducer (BMO-MXene), capable of inhibiting OC progression through the sonodynamic-ferroptosis-immunogenic cell death pathway.© 2024. The Author(s).