Interest in therapies that influence cell senescence to regulate cancer cell is increasing. However, the understanding of the prolonged state of senescent cells and the interactions involved when utilizing therapies that promote senescence alongside other techniques to suppress cancer progression is limited. This study introduces an innovative artificial nanozyme named MVPR, constructed from vanadium MXene (Mo4VC4) combined with the cyclin‐dependent kinase inhibitors Palbociclib and Arg‐Gly‐Asp, for the precise targeting of cancer cell membranes. Within the tumor environment, MVPR initiates a cascade of catalytic reactions, boosting glutathione consumption, generating reactive oxygen species (ROS). When the damage from ROS exceeds the cellular repair capabilities, the redox balance of tumor cells is disrupted, resulting in cell apoptosis. Alternatively, cancer cell senescence can be triggered under different circumstances. Senescent cancer cells impede their own and nearby cancer cell growth by releasing cytokines, thereby effectively curtail uncontrolled proliferation. Furthermore, the immune response triggered by senescent cell recruitment and the response evoked by metal ions in MVPR together enhance the immunotherapeutic effect, boosting immune system activity and augmenting CD4+/CD8+ T cell proliferation. Cancer cells are effectively eliminated through the combined actions of pro‐senescence, enzyme catalysis, and immunogenic response. This study proposes a pro‐senescence strategy for anti‐tumor therapy.

中文翻译：

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一种基于 Mo4VC4 的精确纳米药物，通过利用衰老诱导和免疫原性反应有效消除癌症


人们对影响细胞衰老以调节癌细胞的疗法的兴趣正在增加。然而，对衰老细胞的延长状态以及利用促进衰老的疗法与其他技术抑制癌症进展时所涉及的相互作用的理解是有限的。本研究介绍了一种名为 MVPR 的创新人工纳米酶，它由钒 MXene （Mo4VC4） 与细胞周期蛋白依赖性激酶抑制剂 Palbociclib 和 Arg-Gly-Asp 结合构建，用于精确靶向癌细胞膜。在肿瘤环境中，MVPR 引发一连串催化反应，促进谷胱甘肽消耗，产生活性氧 （ROS）。当 ROS 的损伤超过细胞修复能力时，肿瘤细胞的氧化还原平衡被破坏，导致细胞凋亡。或者，癌细胞衰老可以在不同情况下触发。衰老的癌细胞通过释放细胞因子来阻碍自身和附近的癌细胞生长，从而有效抑制不受控制的增殖。此外，衰老细胞募集触发的免疫反应和 MVPR 中金属离子诱发的反应共同增强了免疫治疗效果，增强了免疫系统活性并增强了 CD4+/CD8+ T 细胞增殖。通过促衰老、酶催化和免疫原性反应的联合作用，癌细胞被有效消除。本研究提出了一种抗肿瘤治疗的促衰老策略。