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已发表论文
通过富铜黑磷纳米平台重编程肿瘤微环境以实现铜死亡敏感的低剂量放射免疫治疗
Authors Chen Y, Wang J , Zheng D, Zhang W
Received 16 September 2025
Accepted for publication 28 November 2025
Published 5 December 2025 Volume 2025:20 Pages 14551—14569
DOI https://doi.org/10.2147/IJN.S563439
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Kamakhya Misra
Yutong Chen,1,* Jin Wang,2,* Daniel Zheng,1,3 Weiyu Zhang3
1Department of Oncology, Shengli Clinical Medical College of Fujian Medical University, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian, 350001, People’s Republic of China; 2Department of Prenatal Diagnosis Center, Jinan Maternity and Child Care Hospital Affiliated to Shandong First Medical University, Jinan, 250001, People’s Republic of China; 3Center for Vascular Surgery and Interventional Oncology, Fuzhou University Affiliated Provincial Hospital, Fuzhou, 350001, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Weiyu Zhang, Fuzhou University Affiliated Provincial Hospital, Fuzhou, 350001, People’s Republic of China, Email zhangwy55@alumni.sysu.edu.cn
Objective: Radioimmunotherapy (RIT) is a promising treatment for deep-seated and metastatic tumors, but its efficacy is limited by the immunosuppressive tumor microenvironment (TME) and a narrow therapeutic window. This study aimed to develop a novel nanoplatform to overcome these constraints by simultaneously sensitizing tumors to radiation, inducing cuproptosis, and reprogramming the immunosuppressive TME.
Methods: We engineered a PEGylated copper-loaded black phosphorus nanoplatform (BPNS@Cu-PEG). Its functionality as a radiosensitizer and cuproptosis inducer was evaluated. The mechanisms of TME reprogramming were investigated, including glutathione (GSH) depletion, reactive oxygen species (ROS) amplification, hypoxia alleviation, and M2-to-M1 macrophage repolarization. Furthermore, we systematically evaluated its antitumor immune effects in vitro and in vivo.
Results: BPNS@Cu-PEG was synthesized with a high copper incorporation rate of 93%. In vitro cellular assays confirmed that the internalized nanoplatform effectively induced cuproptosis and immunogenic cell death (ICD) while simultaneously regulating the TME. In vivo, BPNS@Cu-PEG not only potently inhibited tumor progression and stimulated robust antitumor immunity under low-dose radiotherapy but also exhibited an excellent safety profile.
Conclusion: This work establishes a copper-based, low-dose radioimmunotherapy strategy. The BPNS@Cu-PEG nanoplatform presents a viable and potent strategy to counteract radioresistance and promote systemic antitumor immunity, potentially broadening the therapeutic application and safety profile of RIT.
Keywords: radioimmunotherapy, immunogenic cell death, cuproptosis, tumor microenvironment, black phosphorus
1Department of Oncology, Shengli Clinical Medical College of Fujian Medical University, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian, 350001, People’s Republic of China; 2Department of Prenatal Diagnosis Center, Jinan Maternity and Child Care Hospital Affiliated to Shandong First Medical University, Jinan, 250001, People’s Republic of China; 3Center for Vascular Surgery and Interventional Oncology, Fuzhou University Affiliated Provincial Hospital, Fuzhou, 350001, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Weiyu Zhang, Fuzhou University Affiliated Provincial Hospital, Fuzhou, 350001, People’s Republic of China, Email zhangwy55@alumni.sysu.edu.cn
Objective: Radioimmunotherapy (RIT) is a promising treatment for deep-seated and metastatic tumors, but its efficacy is limited by the immunosuppressive tumor microenvironment (TME) and a narrow therapeutic window. This study aimed to develop a novel nanoplatform to overcome these constraints by simultaneously sensitizing tumors to radiation, inducing cuproptosis, and reprogramming the immunosuppressive TME.
Methods: We engineered a PEGylated copper-loaded black phosphorus nanoplatform (BPNS@Cu-PEG). Its functionality as a radiosensitizer and cuproptosis inducer was evaluated. The mechanisms of TME reprogramming were investigated, including glutathione (GSH) depletion, reactive oxygen species (ROS) amplification, hypoxia alleviation, and M2-to-M1 macrophage repolarization. Furthermore, we systematically evaluated its antitumor immune effects in vitro and in vivo.
Results: BPNS@Cu-PEG was synthesized with a high copper incorporation rate of 93%. In vitro cellular assays confirmed that the internalized nanoplatform effectively induced cuproptosis and immunogenic cell death (ICD) while simultaneously regulating the TME. In vivo, BPNS@Cu-PEG not only potently inhibited tumor progression and stimulated robust antitumor immunity under low-dose radiotherapy but also exhibited an excellent safety profile.
Conclusion: This work establishes a copper-based, low-dose radioimmunotherapy strategy. The BPNS@Cu-PEG nanoplatform presents a viable and potent strategy to counteract radioresistance and promote systemic antitumor immunity, potentially broadening the therapeutic application and safety profile of RIT.
Keywords: radioimmunotherapy, immunogenic cell death, cuproptosis, tumor microenvironment, black phosphorus