免疫系统
免疫原性细胞死亡
肿瘤微环境
奥沙利铂
癌症研究
前药
脂质体
化学
药理学
免疫疗法
医学
免疫学
癌症
生物化学
内科学
结直肠癌
作者
Xianglei Fu,Yanbin Shi,Hengchang Zang,Qingjie Wang,Yongjun Wang,Hang Wu,Shengnan Qiu,Hua Shen,Fanyang Mo,Yankun Zhang,Guimei Lin
标识
DOI:10.1016/j.jconrel.2022.04.041
摘要
Some chemotherapy can damage tumor cells, releasing damage-related molecular patterns including ATP to improve immunological recognition against the tumor by immunogenic cell death (ICD). However, the immune-stimulating ATP may be rapidly degraded into immunosuppressive adenosine by highly expressed CD39 and CD73 in the tumor microenvironment, which leads to immune escape. Based on the above paradox, a liposome nanoplatform combined with ICD inducer (oxaliplatin) and CD39 inhibitor (POM-1) is designed for immunochemotherapy. The liposomes efficiently load the phospholipid-like oxaliplatin prodrug, and the cationic charged surface could adsorb POM-1. Rationally designed DSPE-PEGn-pep, on the one hand, could cover and hide POM-1 to avoid systematic toxicity and, on the other, achieve a response and charge reversal to favor POM-1 shedding and tumor deep penetration. This combination maximizes the ICD effect, and takes two-pronged advantage of stimulating the immune response and relieving immune suppression. The designed POL can effectively inhibit the growth of in situ, lung metastasis and postoperative recurrence melanoma model and form long-term immune memory. With the powerful clinical transformation potential of nanoliposome platforms, this new synergistic strategy is expected to enhance anticancer effects safely and effectively.
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