当前位置：
X-MOL 学术
›
Adv. Funct. Mater.
›
论文详情
Our official English website, www.x-mol.net, welcomes your
feedback! (Note: you will need to create a separate account there.)
Cuproptosis-Driven Enhancement of Thermotherapy by Sequentially Response Cu2-xSe via Copper Chemical Transition
Advanced Functional Materials ( IF 18.5 ) Pub Date : 2023-05-01 , DOI: 10.1002/adfm.202302054 Leung Chan 1, 2 , Yongkang Liu 1 , Muhe Chen 1 , Yanhong Su 1 , Junxian Guo 2 , Liwen Zhu 2 , Meixiao Zhan 1 , Tianfeng Chen 1, 2 , Ligong Lu 1
Advanced Functional Materials ( IF 18.5 ) Pub Date : 2023-05-01 , DOI: 10.1002/adfm.202302054 Leung Chan 1, 2 , Yongkang Liu 1 , Muhe Chen 1 , Yanhong Su 1 , Junxian Guo 2 , Liwen Zhu 2 , Meixiao Zhan 1 , Tianfeng Chen 1, 2 , Ligong Lu 1
Affiliation
|
Activation of cuproptosis pathway has been reported to hold great potential in the application of tumor treatment. But the efficacy of cuproptosis seriously limited by the insufficient accumulation in the tumor sites. Therefore, herein based on the strong stabilization effects of the metalloid element selenium (Se) on copper (Cu), a photothermic Cu2-xSe nanoparticle encapsulated with bioresponsive dimethyl maleic anhydride (DMMA@Cu2-xSe) as a copper-carrier to improve the copper accumulation in tumor is constructed, thus achieving cuproptosis-driven enhancement of thermotherapy. This nanosystem exhibits the enhancement of tumor cellular uptake by a weak acid-triggered charge-switching ability. Next step, the exposed Cu2-xSe is oxidized and releases divalent copper by high-level oxide. Then, the abundant copper induces more dihydrolipoamide S-acetyltransferase oligomerization to down-regulate FDX1 and tricarboxylic acid cycle-related proteins, which leads to inhibiting aerobic respiration. Cuproptosis-induced mitochondrial damage further improves thermotherapy by up-regulating reactive oxygen species (ROS). In addition, the generated ROS also promotes copper release to strengthen cuproptosis, and eventually improves tumor thermotherapy in turn. In general, DMMA@Cu2-xSe with sequentially triggered copper-release, efficient cuproptosis, and appropriate photothermal is a self-enhanced nanoplatform for cuproptosis-driven enhancement of thermotherapy.
中文翻译：
Cuprotosis 驱动的热疗增强，通过铜化学转变顺序响应 Cu2-xSe
据报道，铜凋亡途径的激活在肿瘤治疗的应用中具有巨大的潜力。但铜凋亡的疗效由于在肿瘤部位的积累不足而受到严重限制。因此，本文基于准金属元素硒（Se）对铜（Cu）的强稳定作用，设计了一种生物响应性二甲基马来酸酐封装的光热Cu 2- x Se纳米粒子（DMMA@Cu 2- x Se）作为铜-构建了改善肿瘤内铜积累的载体，从而实现了铜凋亡驱动的热疗增强。该纳米系统通过弱酸触发的电荷转换能力表现出增强肿瘤细胞摄取的能力。下一步，暴露的 Cu 2- xSe被氧化并通过高级氧化物释放二价铜。然后，丰富的铜诱导更多的二氢硫辛酰胺S-乙酰转移酶寡聚化，下调FDX1和三羧酸循环相关蛋白，从而抑制有氧呼吸。铜中毒引起的线粒体损伤通过上调活性氧 (ROS) 进一步改善热疗。此外，产生的ROS还促进铜释放，强化铜凋亡，最终反过来改善肿瘤热疗。一般来说，DMMA@Cu 2- x Se 具有顺序触发的铜释放、高效的铜凋亡和适当的光热，是一种自我增强的纳米平台，用于铜凋亡驱动的热疗增强。
更新日期：2023-05-01
中文翻译：
Cuprotosis 驱动的热疗增强，通过铜化学转变顺序响应 Cu2-xSe
据报道，铜凋亡途径的激活在肿瘤治疗的应用中具有巨大的潜力。但铜凋亡的疗效由于在肿瘤部位的积累不足而受到严重限制。因此，本文基于准金属元素硒（Se）对铜（Cu）的强稳定作用，设计了一种生物响应性二甲基马来酸酐封装的光热Cu 2- x Se纳米粒子（DMMA@Cu 2- x Se）作为铜-构建了改善肿瘤内铜积累的载体，从而实现了铜凋亡驱动的热疗增强。该纳米系统通过弱酸触发的电荷转换能力表现出增强肿瘤细胞摄取的能力。下一步，暴露的 Cu 2- xSe被氧化并通过高级氧化物释放二价铜。然后，丰富的铜诱导更多的二氢硫辛酰胺S-乙酰转移酶寡聚化，下调FDX1和三羧酸循环相关蛋白，从而抑制有氧呼吸。铜中毒引起的线粒体损伤通过上调活性氧 (ROS) 进一步改善热疗。此外，产生的ROS还促进铜释放，强化铜凋亡，最终反过来改善肿瘤热疗。一般来说，DMMA@Cu 2- x Se 具有顺序触发的铜释放、高效的铜凋亡和适当的光热，是一种自我增强的纳米平台，用于铜凋亡驱动的热疗增强。
京公网安备 11010802027423号