文献类型：期刊文献

英文题名：Lipid-Encapsulated Engineered Bacterial Living Materials Inhibit Cyclooxygenase II to Enhance Doxorubicin Toxicity

作者：Jiang, Ning[1,2];Ding, Wanqing[1,2];Zhu, Xiaojuan[1,2];Chen, Jianshu[1,2];Yang, Lin[3];Yi, Xiaoping[1];Zhuang, Yingping[1,2];Qian, Jiangchao[1];Huang, Jiaofang[1,3]

机构：[1]East China Univ Sci & Technol ECUST, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]East China Univ Sci & Technol, Shanghai Collaborat Innovat Ctr Biomfg SCICB, Shanghai 200237, Peoples R China;[3]Jiangxi Normal Univ JXNU, Coll Life Sci, Nanchang 330022, Peoples R China

年份：2024

卷号：6

外文期刊名：BIODESIGN RESEARCH

收录：WOS:【ESCI(收录号:WOS:001267575800001)】；

基金：This work was supported by the National Key Research and Development Program of China (grant no. 2020-YFA0908900) , the Natural Science Foundation of Shanghai (grant no. 22ZR1416000) , the Fundamental Research Funds for Central Universities, and the Open Funding Project of State Key Laboratory of Microbial Metabolism (grant no. MMLKF24-01) .

语种：英文

外文关键词：Doxorubicin Toxicity. BioDesign Res.; Exclusive licensee Nanjing

摘要：Recently, there has been increasing interest in the use of bacteria for cancer therapy due to their ability to selectively target tumor sites and inhibit tumor growth. However, the complexity of the interaction between bacteria and tumor cells evokes unpredictable therapeutic risk, which induces inflammation, stimulates the up-regulation of cyclooxygenase II (COX-2) protein, and stimulates downstream antiapoptotic gene expression in the tumor microenvironment to reduce the antitumor efficacy of chemotherapy and immunotherapy. In this study, we encapsulated celecoxib (CXB), a specific COX-2 inhibitor, in liposomes anchored to the surface of Escherichia coli Nissle 1917 (ECN) through electrostatic absorption (C@ECN) to suppress ECN-induced COX-2 up-regulation and enhance the synergistic antitumor effect of doxorubicin (DOX). C@ECN improved the antitumor effect of DOX by restraining COX-2 expression. In addition, local T lymphocyte infiltration was induced by the ECN to enhance immunotherapy efficacy in the tumor microenvironment. Considering the biosafety of C@ECN, a hypoxia-induced lysis circuit, pGEX-Pvhb-Lysis, was introduced into the ECN to limit the number of ECNs in vivo. Our results indicate that this system has the potential to enhance the synergistic effect of ECN with chemical drugs to inhibit tumor progression in medical oncology.