Journal
BIOMATERIALS
Volume 90, Issue -, Pages 72-84Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.biomaterials.2016.03.009
Keywords
Tumor-associated macrophage; Tumor-infiltrating dendritic cell; Targeted delivery; Let-7b; Cancer immunotherapy
Funding
- National Science Fund for Distinguished Young Scholars [81025019]
- National Basic Research Program of China [2012CB517603]
- National High Technology Research and Development Program of China [2014AA020707]
- Program for New Century Excellent Talents in University [NCET-13-0272]
- National Natural Science Foundation of China [31271013, 31170751, 31200695, 31400671, 31571458, 51173076]
- Ph.D. Programs Foundation of the Ministry of Education of China [20130091110037]
- China Postdoctoral Science Foundation [2014M551555, 2015T80536]
- Macao Science and Technology Fund [FDCT048/2013/A2]
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Both tumor associated macrophages (TAMs) and tumor infiltrating dendritic cells (TIDCs) are important components in the tumor microenvironment that mediate tumor immunosuppression and promote cancer progression. Targeting these cells and altering their phenotypes may become a new strategy to recover their anti-tumor activities and thereby restore the local immune surveillance against tumor. In this study, we constructed a nucleic acid delivery system for the delivery of let-7b, a synthetic microRNA mimic. Our carrier has an affinity for the mannose receptors on TAMs/TIDCs and is responsive to the low pH tumor microenvironment. The delivery of let-7b could reactivate TAMs/TIDCs by acting as a TLR-7 agonist and suppressing IL-10 production in vitro. In a breast cancer mouse model, let-7b delivered by this system efficiently reprogrammed the functions of TAMs/TIDCs, reversed the suppressive tumor microenvironment, and inhibited tumor growth. Taken together, this strategy, designed based upon TAMs/TIDCs-targeting delivery and the dual biological functions of let-7b (TLR-7 ligand and IL-10 inhibitor), may provide a new approach for cancer immunotherapy. (C) 2016 Elsevier Ltd. All rights reserved.
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