Multifunctional biomimetic nanoparticles loading baicalin for polarizing tumor-associated macrophages

Han, Shulan; Wang, Wenjie; Wang, Shengfang; Wang, Shuo; Ju, Rui-Jun; Pan, Zihao; Yang, Tingyuan; Zhang, Guifeng; Wang, Huimei; Wang, Lianyan

doi:10.1039/c9nr03353j

Cited by 60 publications

(26 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several studies have demonstrated that nanodrugs offer superiority in mediating the polarization of macrophages with increased drug uptake. For instance, curcumin (cur), baicalin (Bai), and ginseng-derived nanoparticles have been reported to alter TaM polarization without discernible toxicity (90)(91)(92). compared to the drugs themselves, their nanoparticle derivatives showed improved pharmacokinetics and bioavailability in systemic circulation, and thus contributed toward excellent antitumor responses (90)(91)(92).…”

Section: Tam-targeted Therapeuticsmentioning

confidence: 99%

“…For instance, curcumin (cur), baicalin (Bai), and ginseng-derived nanoparticles have been reported to alter TaM polarization without discernible toxicity (90)(91)(92). compared to the drugs themselves, their nanoparticle derivatives showed improved pharmacokinetics and bioavailability in systemic circulation, and thus contributed toward excellent antitumor responses (90)(91)(92). Furthermore, few materials used in nanoparticle production, including Tio 2 and ag, may preferentially polarize TaMs towards an M1 phenotype (93,94).…”

Section: Tam-targeted Therapeuticsmentioning

confidence: 99%

See 1 more Smart Citation

Tumor‑associated macrophages in lung cancer: Friendly or evil? (Review)

Wei

Tang

et al. 2020

Mol Med Rep

View full text Add to dashboard Cite

Typically, tumor-associated macrophages (TaMs), an abundant population of leukocytes in lung cancer, are affected by tumor microenvironment (TMe) and shift towards either a pro-tumor (M2-like) or an anti-tumor phenotype (M1-like). M2-polarized macrophages, are one of the primary tumor-infiltrating immune cells and were reported to be associated with the promotion of cancer cell growth, invasion, metastasis, and angiogenesis. TaMs are considered a potential target for adjuvant anticancer therapies, and recent therapeutic approaches targeting the M2 polarization of TaMs have shown encouraging results. The present review discusses recent developments in the role of TaMs in cancer, in particular TaMs functions, clinical implication and prospective therapeutic strategies in lung cancer. Contents 1. introduction 2. Macrophage plasticity in lung cancer development 3. Functional aspects of macrophages in lung cancer 4. clinical implications of TaMs in lung cancer 5. TaM-targeted therapeutics 6. conclusions

show abstract

Section: Tam-targeted Therapeuticsmentioning

confidence: 99%

Section: Tam-targeted Therapeuticsmentioning

confidence: 99%

Tumor‑associated macrophages in lung cancer: Friendly or evil? (Review)

Wei

Tang

et al. 2020

Mol Med Rep

View full text Add to dashboard Cite

show abstract

“…Their shift between the classically activated (M1, proinflammatory) and alternatively activated (M2, anti-inflammatory) phenotypes has been recognized as a crucial factor in the initiation, progression, and termination of numerous inflammatory diseases (Zhang et al, 2018) and especially in influenza virus infection (Halstead et al, 2018). Modulation of macrophage polarization has previously been shown to inhibit or promote influenza infection by applying GM-CSF (Sun et al, 2018) or Afatoxin B1 (Han et al, 2019), respectively. In this study, we confirm that the high mortality of infected mice is correlated with an abundant recruitment of macrophages to the lung and a high proportion of M1-polarized macrophages.…”

Section: Discussionmentioning

confidence: 99%

Baicalin Inhibits Influenza A Virus Infection via Promotion of M1 Macrophage Polarization

et al. 2020

View full text Add to dashboard Cite

Background and Aims: The natural compound baicalin (BA) possesses potent antiviral properties against the influenza virus. However, the underlying molecular mechanisms of this antiviral activity and whether macrophages are involved remain unclear. In this study, we, therefore, investigated the effect of BA on macrophages. Methods: We studied macrophage recruitment, functional phenotypes (M1/M2), and the cellular metabolism via flow cytometry, qRT-PCR, immunofluorescence, a cell culture transwell system, and GC-MS-based metabolomics both in vivo in H1N1 A virus-infected mice and in vitro. Results: BA treatment drastically reduced macrophage recruitment (CD11b + , F4/80 +) by approximately 90% while maintaining the proportion of M1-polarized macrophages in the bronchoalveolar lavage fluid of infected mice. This BA-stimulated macrophage M1 phenotype shift was further verified in vitro in ANA-1 and primary peritoneal macrophages by measuring macrophage M1 polarization signals (CD86, iNOS, TNF-a, iNOS/Arg-1 ratio, and IL-1b cleavage). Meanwhile, we observed an activation of the IFN pathway (upregulation of IFN-b and IRF-3), an inhibition of influenza virus replication (as measured by the M gene), and distinct cellular metabolic responses in BA-treated cells. Conclusion: BA triggered macrophage M1 polarization, IFN activation, and other cellular reactions, which are beneficial for inhibition of H1N1 A virus infection.

show abstract

“…NPs were further entrapped in a galactose-modified erythrocyte coating to increase biocompatibility and TAM targeting, the macrophage galactose-type lectin (MGL; CD301) receptor is expressed on myeloid antigen-presenting cells including macrophages. These biomimetic NPs also suppressed melanoma growth in vivo and increased the infiltration of CD8+ T cells into the TME [40].…”

Section: Reprogramming the Immunosuppressive Tme With Nanotherapeuticsmentioning

confidence: 93%

Exploiting Current Understanding of Hypoxia Mediated Tumour Progression for Nanotherapeutic Development

Feng

Byrne

Jamal

et al. 2019

Cancers

View full text Add to dashboard Cite

Hypoxia is one of the most common phenotypes of malignant tumours. Hypoxia leads to the increased activity of hypoxia-inducible factors (HIFs), which regulate the expression of genes controlling a raft of pro-tumour phenotypes. These include maintenance of the cancer stem cell compartment, epithelial-mesenchymal transition (EMT), angiogenesis, immunosuppression, and metabolic reprogramming. Hypoxia can also contribute to the tumour progression in a HIF-independent manner via the activation of a complex signalling network pathway, including JAK-STAT, RhoA/ROCK, NF-κB and PI3/AKT. Recent studies suggest that nanotherapeutics offer a unique opportunity to target the hypoxic microenvironment, enhancing the therapeutic window of conventional therapeutics. In this review, we summarise recent advances in understanding the impact of hypoxia on tumour progression, while outlining possible nanotherapeutic approaches for overcoming hypoxia-mediated resistance.

show abstract

Multifunctional biomimetic nanoparticles loading baicalin for polarizing tumor-associated macrophages

Abstract: Immunosuppression and immune tolerance lead tumor cells to evade immune system surveillance and weaken drug efficacy.

Cited by 60 publications

References 46 publications

Tumor‑associated macrophages in lung cancer: Friendly or evil? (Review)

Tumor‑associated macrophages in lung cancer: Friendly or evil? (Review)

Baicalin Inhibits Influenza A Virus Infection via Promotion of M1 Macrophage Polarization

Exploiting Current Understanding of Hypoxia Mediated Tumour Progression for Nanotherapeutic Development

Contact Info

Product

Resources

About