Abstract:Supporting InformationThe Supporting Information is available free of charge at https://pubs.acs.org/doi/10.1021/acsnano.9b04571. Further polymer characterization, in vitro BTNP behavior, pharmacokinetic parameters and mouse model results (PDF)
“…According to the location of the tumor cells, we could divide the strategies into primary cancer targeting drug delivery and cancer metastasis-targeting drug delivery ( Fig. 1 and Table 1 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 ). Figure 1 Targeting drug delivery strategies for tumor metastasis treatment.…”
Section: Cancer Targeting Drug Deliverymentioning
confidence: 99%
“… 29 Dual-targeting tumor and other cells in metastasis Folic acid and alendronate-modified PLGA nanoparticles could dual-target bone mass and tumor cells in bone metastasis. 30 Modulating pre-metastasis niche S100A4 siRNA-loaded exosome could downregulate the expression of S100A4 in lung fibroblast, which significantly reduce breast cancer lung metastasis. 31 Hijacking circulating cells Hijacking platelet P-Selectin-modified redox-responsive paclitaxel-loaded micelle (PSN-PEG-SS-PTX4) could bind with activated platelet in circulation and then target to lung metastasis.…”
As one of the most serious threats to human being, cancer is hard to be treated when metastasis happens. What's worse, there are few identified targets of metastasis for drug development. Therefore, it is important to develop strategies to prevent metastasis or treat existed metastasis. This review focuses on the procedure of metastasis, and first summarizes the targeting delivery strategies, including primary tumor targeting drug delivery, tumor metastasis targeting drug delivery and hijacking circulation cells. Then, as a promising treatment, the application of immunotherapy in tumor metastasis treatment is introduced, and strategies that stimulating immune response are reviewed, including chemotherapy, photothermal therapy, photodynamic therapy, ferroptosis, sonodynamic therapy, and nanovaccines. Finally, the challenges and perspective about nanoparticle-enabled tumor metastasis treatment are discussed.
“…According to the location of the tumor cells, we could divide the strategies into primary cancer targeting drug delivery and cancer metastasis-targeting drug delivery ( Fig. 1 and Table 1 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 ). Figure 1 Targeting drug delivery strategies for tumor metastasis treatment.…”
Section: Cancer Targeting Drug Deliverymentioning
confidence: 99%
“… 29 Dual-targeting tumor and other cells in metastasis Folic acid and alendronate-modified PLGA nanoparticles could dual-target bone mass and tumor cells in bone metastasis. 30 Modulating pre-metastasis niche S100A4 siRNA-loaded exosome could downregulate the expression of S100A4 in lung fibroblast, which significantly reduce breast cancer lung metastasis. 31 Hijacking circulating cells Hijacking platelet P-Selectin-modified redox-responsive paclitaxel-loaded micelle (PSN-PEG-SS-PTX4) could bind with activated platelet in circulation and then target to lung metastasis.…”
As one of the most serious threats to human being, cancer is hard to be treated when metastasis happens. What's worse, there are few identified targets of metastasis for drug development. Therefore, it is important to develop strategies to prevent metastasis or treat existed metastasis. This review focuses on the procedure of metastasis, and first summarizes the targeting delivery strategies, including primary tumor targeting drug delivery, tumor metastasis targeting drug delivery and hijacking circulation cells. Then, as a promising treatment, the application of immunotherapy in tumor metastasis treatment is introduced, and strategies that stimulating immune response are reviewed, including chemotherapy, photothermal therapy, photodynamic therapy, ferroptosis, sonodynamic therapy, and nanovaccines. Finally, the challenges and perspective about nanoparticle-enabled tumor metastasis treatment are discussed.
“…One possible mechanism may include phagocytic cell uptake as described in the “ELVIS” effect (extravasation via leaky vasculature followed by inflammatory cell sequestration) 43,44 . Nevertheless, modifications to the nanoparticle chemistry have shown enhanced retention at target sites and allow for further improvement of nanoparticle accumulation in bone in other disease models 29 . Considering that sites of inflammation and infection are known to produce ROS 45 and that release of compounds from PPS nanoparticles is responsive to ROS concentration, it is likely that ROS levels at infected sites contribute to drug cargo release within bone.…”
Section: Discussionmentioning
confidence: 99%
“…DMA was purified by distillation under reduced pressure before polymerization. PPS (10 kDa), poly(propylene sulfide)‐4‐cyano‐4‐(ethylsulfanylthiocarbonyl)sulfanylpentanoic acid (PPS 135 ‐ECT), and poly(benzoyloxypropyl methacrylamide) (pHPMA‐Bz) were synthesized as described previously 29 …”
Osteomyelitis is a debilitating infection of bone that results in substantial morbidity. Staphylococcus aureus is the most commonly isolated pathogen causing bone infections and features an arsenal of virulence factors that contribute to bone destruction and counteract immune responses. We previously demonstrated that diflunisal, a nonsteroidal anti-inflammatory drug, decreases S. aureus-induced bone destruction during osteomyelitis when delivered locally from a resorbable drug delivery depot. However, local diflunisal therapy was complicated by bacterial colonization of the depot's surface, highlighting a common pitfall of devices for local drug delivery to infected tissue. It is, therefore, critical to develop an alternative drug delivery method for diflunisal to successfully repurpose this drug as an antivirulence therapy for osteomyelitis. We hypothesized that a nanoparticle-based parenteral delivery strategy would provide a method for delivering diflunisal to infected tissue while circumventing the complications associated with local delivery. In this study, we demonstrate that poly(propylene sulfide) (PPS) nanoparticles accumulate at the infectious focus in a murine model of staphylococcal osteomyelitis and are capable of efficaciously delivering diflunisal to infected bone. Moreover, diflunisal-loaded PPS nanoparticles effectively decrease S. aureus-mediated bone destruction, establishing the feasibility of systemic delivery of an antivirulence compound to mitigate bone pathology during osteomyelitis.
“…In contrast, GANT58 reduced expression of ITGB3 , GLI2 , and PTHRP in tumor cells cultured on both 2D films and bone-like 3D scaffolds, which highlights the potential of Gli2 inhibitors for blocking TIBD. It was recently shown that targeting Gli2 inhibition to the tumor-bone microenvironment effectively reduced TIBD in a model of breast cancer metastasis to bone [ 57 , 58 ]. Thus, this study emphasizes the importance of studying tumor cell signaling and response to therapeutics in 3D cultures that accurately capture the physical properties of the bone microenvironment.…”
Patients with advanced skeletal metastases arising from primary cancers including breast, lung, and prostate suffer from extreme pain, bone loss, and frequent fractures. While the importance of interactions between bone and tumors is well-established, our understanding of complex cell–cell and cell–microenvironment interactions remains limited in part due to a lack of appropriate 3D bone models. To improve our understanding of the influence of bone morphometric properties on the regulation of tumor-induced bone disease (TIBD), we utilized bone-like 3D scaffolds in vitro and in vivo. Scaffolds were seeded with tumor cells, and changes in cell motility, proliferation, and gene expression were measured. Genes associated with TIBD significantly increased with increasing scaffold rigidity. Drug response differed when tumors were cultured in 3D compared to 2D. Inhibitors for Integrin β3 and TGF-β Receptor II significantly reduced bone-metastatic gene expression in 2D but not 3D, while treatment with the Gli antagonist GANT58 significantly reduced gene expression in both 2D and 3D. When tumor-seeded 3D scaffolds were implanted into mice, infiltration of myeloid progenitors changed in response to pore size and rigidity. This study demonstrates a versatile 3D model of bone used to study the influence of mechanical and morphometric properties of bone on TIBD.
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