Lyu Lijuan, Yi Ming, Chen Ji, Zhang Jing, Ma Xiaobin, Zhang Xiaojun, Zeng Liang, Xue Yan, Wen Haimei, Deng Yujiao, Zhou Pengfei, Wu Kongming, Kang Huafeng, Dai Zhijun
The Comprehensive Breast Care Center, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.
Department of Breast Surgery, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310000, China.
Adv Sci (Weinh). 2025 Aug;12(30):e01819. doi: 10.1002/advs.202501819. Epub 2025 Jun 5.
Beyond inherently killing cancer cells by directly inducing double-strand DNA breaks, local radiotherapy (RT) can exert immune-priming effects and reprogram the tumor microenvironment (TME) from immune-cold tumors into inflamed, or "hot" tumors. Nevertheless, this immunogenic antitumor response may be partially counterbalanced by the upregulation of vascular endothelial growth factor (VEGF) and transforming growth factor-beta (TGF-β) induced by RT. Y332D, a bispecific antibody that simultaneously blockades VEGF and TGF-β, effectively synergized with RT, leading to a durable antitumor effect. Mechanistically, Y332D counteracted negative RT effects that are attributed to the upregulation of TGF-β and VEGF-mediated epithelial-mesenchymal transition, extracellular matrix remodeling, aberrant angiogenesis, immunosuppression, and radioresistance, as well as further enhanced or complemented the positive effects of RT, such as cGAS-STING activation, immunogenic cell death, enhanced antigen presentation, increased T cell infiltration, and antiangiogenic effects, thereby reprograming the TME from immune "cold" to inflamed state and forming an effective in-situ vaccine that, beyond local tumor eradication, could potentiate antitumor immune response and regress preestablished abscopal metastases. Together, our results indicate that this combination strategy successfully overcame the negative effects caused by RT and augmented abscopal effects, extending the application of RT to the treatment of both local and metastatic disease.
除了通过直接诱导双链DNA断裂来固有地杀死癌细胞外,局部放射治疗(RT)还可以发挥免疫启动作用,并将肿瘤微环境(TME)从免疫冷肿瘤重编程为炎症性或“热”肿瘤。然而,这种免疫原性抗肿瘤反应可能会被RT诱导的血管内皮生长因子(VEGF)和转化生长因子-β(TGF-β)的上调部分抵消。Y332D是一种同时阻断VEGF和TGF-β的双特异性抗体,与RT有效协同作用,产生持久的抗肿瘤效果。从机制上讲,Y332D抵消了RT的负面效应,这些负面效应归因于TGF-β上调和VEGF介导的上皮-间质转化、细胞外基质重塑、异常血管生成、免疫抑制和放射抗性,以及进一步增强或补充了RT的正面效应,如cGAS-STING激活、免疫原性细胞死亡、增强抗原呈递、增加T细胞浸润和抗血管生成作用,从而将TME从免疫“冷”状态重编程为炎症状态,并形成一种有效的原位疫苗,除了根除局部肿瘤外,还可以增强抗肿瘤免疫反应并使预先建立的远隔转移消退。总之,我们的结果表明,这种联合策略成功克服了RT引起的负面影响并增强了远隔效应,将RT的应用扩展到局部和转移性疾病的治疗。