纳米酶催化治疗研究数据集

（1）合成了PEG-GO@XN纳米酶复合材料。药物在PEG-GO纳米片表面上的负载可受到精确控制。原子力显微镜表征表明EG-GO@XN纳米复合材料的平均直径为~100 nm，平均厚度为~2 nm，比PEG-GO纳米片（~1.6 nm）略厚，这可能归因于XN分子连接在纳米片的两侧所致。PEG-GO@XN纳米酶复合材料还具有良好的生物相容性，即便在较高浓度下也无显著细胞毒性。（2）为了确定低浓度PEG-GO@XN纳米酶复合材料对细胞能量代谢的影响，利用Seahorse XF24-3细胞外通量分析仪实时测量了胞内氧化磷酸化水平。对线粒体氧化磷酸化有明显的抑制作用；而对乳腺癌上皮细胞MCF-10A的影响不明显，提示PEG-GO@XN在体外显著抑制了乳腺癌细胞线粒体氧化磷酸化并减少乳腺癌细胞中ATP的产生，免疫荧光成像实验表明PEG-GO@XN纳米酶复合材料阻遏了细胞板状伪足区域中F-肌动蛋白细胞骨架的形成。（3）通过动物实验进一步研究了PEG-GO@XN纳米酶复合材料对肿瘤细胞肺转移能力的影响，结果表明，PEG-GO@XN可以显著降低裸鼠中MDA-MB-231细胞的肺转移活性。肿瘤细胞经常通过发生内皮-间质转化（EMT）以获得侵袭能力。在发生EMT时，细胞失去粘附的上皮特征并获得迁移性间充质特征，以能够更有效地迁移并侵袭周边的间质。EMT与肿瘤发生、转移和对治疗的抗性相关。机制研究表明PEG-GO@XN显著抑制了MDA-MB-231乳腺癌细胞中诱导EMT的转录因子Snail和Twist的表达。PEG-GO@XN也可能通过阻断Snail介导的转录抑制作用减弱了E-钙粘蛋白的下调，提示PEG-GO@XN纳米酶复合材料抑制乳腺癌细胞的EMT过程，从而维持乳腺癌细胞的“紧密上皮型”表型而非“间质样”特征，从而降低了乳腺癌细胞的运动潜能。

(1) The PEG-GO@XN nanozyme composite was synthesized. The loading of drugs on the surface of PEG-GO nanosheets can be precisely controlled. Atomic force microscopy (AFM) characterization showed that the average diameter of PEG-GO@XN nanocomposites was ~100 nm, with an average thickness of ~2 nm, which was slightly thicker than that of PEG-GO nanosheets (~1.6 nm). This may be attributed to the attachment of XN molecules on both sides of the nanosheets. The PEG-GO@XN nanozyme composite also exhibited excellent biocompatibility, with no significant cytotoxicity even at relatively high concentrations.
(2) To investigate the effect of low-concentration PEG-GO@XN nanozyme composites on cellular energy metabolism, the intracellular oxidative phosphorylation level was measured in real-time using a Seahorse XF24-3 Extracellular Flux Analyzer. PEG-GO@XN exhibited significant inhibitory effect on mitochondrial oxidative phosphorylation, while showed negligible effects on breast epithelial MCF-10A cells, suggesting that PEG-GO@XN significantly inhibits mitochondrial oxidative phosphorylation and reduces ATP production in breast cancer cells in vitro. Immunofluorescence imaging experiments further demonstrated that PEG-GO@XN nanozyme composites suppressed the formation of F-actin cytoskeleton in the lamellipodia regions of cells.
(3) The effect of PEG-GO@XN nanozyme composites on the lung metastatic capacity of tumor cells was further investigated via animal experiments, and the results showed that PEG-GO@XN significantly reduced the lung metastatic activity of MDA-MB-231 cells in nude mice. Tumor cells often acquire invasive capacity through epithelial-mesenchymal transition (EMT). During EMT, cells lose adhesive epithelial characteristics and acquire migratory mesenchymal features, enabling more efficient migration and invasion of surrounding stroma. EMT is associated with tumorigenesis, metastasis, and therapeutic resistance. Mechanistic studies revealed that PEG-GO@XN significantly inhibited the expression of Snail and Twist, the transcription factors that induce EMT, in MDA-MB-231 breast cancer cells. PEG-GO@XN may also attenuate the downregulation of E-cadherin by blocking Snail-mediated transcriptional repression, suggesting that PEG-GO@XN nanozyme composites suppress the EMT process of breast cancer cells, thereby maintaining the "tight epithelial" phenotype rather than the "mesenchymal-like" characteristics of breast cancer cells, and thus reducing the migratory potential of breast cancer cells.

搜集汇总

背景与挑战

背景概述

该数据集围绕PEG-GO@XN纳米酶复合材料的合成与表征展开，其具有良好的生物相容性。研究通过体外和体内实验表明，该材料能抑制乳腺癌细胞的能量代谢和肺转移，并阻断EMT过程，从而降低肿瘤细胞的运动潜能。