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• W4317481502 abstract "Immunotherapy has been regarded as a breakthrough in cancer treatment and achieved great success. However, the poor response rate is still a formidable challenge of current immunotherapies, especially in solid tumors without sufficient infiltration of immune cells, also known as cold tumor. SAR405 is a highly specific VPS34 inhibitor and has been suggested as a potential approach converting cold tumor into hot tumor by inhibiting autophagy. In this study, a tri-functional doxorubicin (DOX) plus SAR405 liposome system is established and further modified with a novel anti-PD-L1 peptide JY4 for targeted delivery (DOX-SAR-JY4LIPO ). The data here demonstrate that in a lung cancer xenograft mouse model, by facilitating the tumoral enrichment of both SAR405 and DOX, DOX-SAR-JY4LIPO effectively increases the infiltration of cytotoxic lymphocytes in the tumor by synergizing DOX-induced immunogenic cell death (ICD) and SAR405-mediated upregulation of chemokines including CCL5 and CXCL10. As results, DOX-SAR-JY4LIPO significantly inhibits tumor growth, metastasis, and resurrection by re-educating immunosuppressive tumor microenvironment. In conclusion, this study not only proves the concept of inhibiting autophagy for better immune infiltration in the tumor but also presents a novel tri-functional liposomal system that overcomes the deficiencies of current therapies and holds great promise in cancer immunotherapy." @default.
• W4317481502 created "2023-01-20" @default.
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• W4317481502 date "2023-02-03" @default.
• W4317481502 modified "2023-10-15" @default.
• W4317481502 title "A Novel Tri‐Functional Liposome Re‐Educates “Cold Tumor” and Abrogates Tumor Growth by Synergizing Autophagy Inhibition and PD‐L1 Blockade" @default.
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• W4317481502 doi "https://doi.org/10.1002/adhm.202202757" @default.
• W4317481502 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36652763" @default.
• W4317481502 hasPublicationYear "2023" @default.
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