Department of Ophthalmology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410013, China.
Department of Ophthalmology, Changde Hospital, Xiangya School of Medicine, Central South University, Changde, Hunan, 415000, China.
Adv Sci (Weinh). 2024 Aug;11(31):e2404375. doi: 10.1002/advs.202404375. Epub 2024 Jun 18.
In the treatment of uveal melanoma (UVM), histone deacetylase inhibitors (HDACi) have emerged as a promising epigenetic therapy. However, their clinical efficacy is hindered by the suboptimal pharmacokinetics and the strong self-rescue of tumor cells. To overcome these limitations, reactive oxygen species (ROS)-responsive nanoparticles (NPs) are designed that encapsulate HDACi MS-275 and the glutamine metabolism inhibitor V-9302. Upon reaching the tumor microenvironment, these NPs can disintegrate, thereby releasing MS-275 to increase the level of ROS and V-9302 to reduce the production of glutathione (GSH) related to self-rescue. These synergistic effects lead to a lethal ROS storm and induce cell pyroptosis. When combined with programmed cell death protein 1 monoclonal antibodies (α-PD-1), these NPs facilitate immune cell infiltration, improving anti-tumor immunity, converting "immune-cold" tumors into "immune-hot" tumors, and enhancing immune memory in mice. The findings present a nano-delivery strategy for the co-delivery of epigenetic therapeutics and metabolic inhibitors, which induces pyroptosis in tumors cells and improves the effectiveness of chemotherapy and immunotherapy.
在葡萄膜黑色素瘤(UVM)的治疗中,组蛋白去乙酰化酶抑制剂(HDACi)作为一种有前途的表观遗传学治疗方法已经出现。然而,其临床疗效受到药代动力学不佳和肿瘤细胞强烈自救的限制。为了克服这些限制,设计了活性氧(ROS)响应纳米颗粒(NPs),其包封了 HDACi MS-275 和谷氨酰胺代谢抑制剂 V-9302。当到达肿瘤微环境时,这些 NPs 会解体,从而释放 MS-275 以增加 ROS 水平,并减少与自救相关的谷胱甘肽(GSH)的产生。这些协同作用导致致命的 ROS 风暴并诱导细胞焦亡。当与程序性细胞死亡蛋白 1 单克隆抗体(α-PD-1)联合使用时,这些 NPs 促进免疫细胞浸润,增强抗肿瘤免疫,将“免疫冷”肿瘤转化为“免疫热”肿瘤,并增强小鼠的免疫记忆。这些发现提出了一种用于共递送表观遗传治疗剂和代谢抑制剂的纳米递药策略,该策略诱导肿瘤细胞发生焦亡,并提高化疗和免疫疗法的效果。