Journal
JOURNAL OF CONTROLLED RELEASE
Volume 296, Issue -, Pages 150-161Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jconrel.2019.01.027
Keywords
Photothermal therapy; Black phosphorus quantum dot; PD-1 antibody; Immune checkpoint blockade; Triple-negative phenotype basal-like breast cancer; Erythrocyte membrane
Funding
- National Natural Science Foundation of China [81771966]
- Fundamental Research Funds for the Central Universities
- Guangdong Natural Science Funds for Distinguished Young Scholar [2014A030306036]
- Natural Science Foundation of Guangdong Province [2015A030313848, 2016A030310023]
- China Podtdoctoral Science Foundation [2017M612742]
- Guangdong Special Support Program [201428030]
- Science and Technology Planning Project of Guangdong Province [2016A020217001, 2014A020212466]
- Science, Technology & Innovation Commission of Shenzhen Municipality [JCYJ20160301152300347, JCYJ20160531195129079, JCYJ20170412095722235, JCYJ20160429171931438, JCY20170818162637217, 2018104246]
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Basal-like breast cancer exhibits a triple-negative phenotype and has a poor prognosis, even with traditional chemical and anti-human epidermal growth factor receptor (HER) treatments. However, the high mutation rate of this obstinate cancer type renders it suitable for immunotherapy. Photothermal therapy (PIT) is a highefficiency method for inducing tumor neoantigen release in situ, which has great potential for use in cancer immunotherapy. Here, we prepared a biomimetic black phosphorus quantum dot (BPQDs) formulation to induce breast cancer cell apoptosis in situ by near-infrared (NIR) laser irradiation to mobilize the immune system to eliminate the residual and metastatic cancer cells. Erythrocyte membranes (RMs) were used to coat the BPQDs, forming a BPQD-RM nanovesicle (BPQD-RMNV) biomimetic formulation that exhibited a long circulation time and tumor accumulation in vivo. The basal-like 4T1 breast tumor underwent apoptosis and necrosis with the irradiation and recruited dendritic cells (DCs) to capture the tumor antigens in vivo. Furthermore, programmed cell death protein 1 (PD-1) antibody (aPD-1) was employed to prevent the CD8(+) T cells from exhaustion. Notably, BPQD-RMNV-mediated PTT combined with aPD-1 treatment significantly delayed residual and metastatic tumor growth in vivo. Hence, BPQD-RMNV-mediated PIT combined with immune checkpoint blockade antibody increased the infiltration and activity of CD8(+) T cells in the tumor, which directly restrained basal-like breast tumor growth in vivo.
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