Synergistic ferroptosis and macrophage re-polarization using engineering exosome-mimic M1 nanovesicles for cancer metastasis suppression

Li, Ping; Gao, Mengqiu; Hu, Zijian; Xu, Tian; Chen, Jieru; Ma, Yuxuan; Li, Siwen; Gu, Yueqing

doi:10.1016/j.cej.2020.128217

Cited by 34 publications

(16 citation statements)

References 39 publications

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“…Attempts have been made to use exosomes as carriers for ferroptosis-inducing drugs to trigger cell death among cancer cells. For example, engineered M1 macrophages, with CCR2 overexpression, are employed as Fe 3 O 4 NP carriers ( Li et al, 2021 ). Moreover, a well-known ferroptosis inducer, erastin, can be loaded into exosomes labeled with folate and delivered to cancer cells that express the folate receptor to generate ROS and glutathione depletion ( Yu et al, 2019 ).…”

Section: Ferroptosis and The Tumor Microenvironmentmentioning

confidence: 99%

Ferroptosis and Cancer: Complex Relationship and Potential Application of Exosomes

Liu

et al. 2021

Front. Cell Dev. Biol.

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Cell death induction has become popular as a novel cancer treatment. Ferroptosis, a newly discovered form of cell death, features regulated, iron-dependent accumulation of lipid hydroperoxides. Since this word “ferroptosis” was coined, numerous studies have examined the complex relationship between ferroptosis and cancer. Here, starting from the intrinsic hallmarks of cancer and cell death, we discuss the theoretical basis of cell death induction as a cancer treatment. We review various aspects of the relationship between ferroptosis and cancer, including the genetic basis, epigenetic modification, cancer stem cells, and the tumor microenvironment, to provide information and support for further research on ferroptosis. We also note that exosomes can be applied in ferroptosis-based therapy. These extracellular vesicles can deliver different molecules to modulate cancer cells and cell death pathways. Using exosomes to control ferroptosis occurring in targeted cells is promising for cancer therapy.

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Section: Ferroptosis and The Tumor Microenvironmentmentioning

confidence: 99%

Ferroptosis and Cancer: Complex Relationship and Potential Application of Exosomes

Liu

et al. 2021

Front. Cell Dev. Biol.

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“…M1 macrophages produce high levels of proinflammatory and immunostimulatory cytokines, including interleukin 12 (IL-12), interleukin 23 (IL-23), tumor necrosis factor alpha (TNFα) etc., leading to tumor suppression [ 23 ]. It has been reported that M1 macrophage-derived exosomes (M1Exo) can release pro-inflammatory signals and generate a stimulatory tumor immune-microenvironment, implying that they have great therapeutic potentials for anti-cancer therapy [ 24 ]. More recently, M1Exo has been used as drug carrier to deliver paclitaxel into the tumor tissue, and results demonstrated that M1Exo provided a pro-inflammatory environment which further enhanced the therapeutic efficacy of chemotherapy by activating the apoptosis pathway [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

M1 Macrophage-Derived Exosomes Loaded with Gemcitabine and Deferasirox against Chemoresistant Pancreatic Cancer

et al. 2021

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Pancreatic cancer is a malignant disease with high mortality and poor prognosis due to lack of early diagnosis and low treatment efficiency after diagnosis. Although Gemcitabine (GEM) is used as the first-line chemotherapeutic drug, chemoresistance is still the major problem that limits its therapeutic efficacy. Here in this study, we developed a specific M1 macrophage-derived exosome (M1Exo)-based drug delivery system against GEM resistance in pancreatic cancer. In addition to GEM, Deferasirox (DFX) was also loaded into drug carrier, M1Exo, in order to inhibit ribonucleotide reductase regulatory subunit M2 (RRM2) expression via depleting iron, and thus increase chemosensitivity of GEM. The M1Exo nanoformulations combining both GEM and DFX significantly enhanced the therapeutic efficacy on the GEM-resistant PANC-1/GEM cells and 3D tumor spheroids by inhibiting cancer cell proliferation, cell attachment and migration, and chemoresistance to GEM. These data demonstrated that M1Exo loaded with GEM and DFX offered an efficient therapeutic strategy for drug-resistant pancreatic cancer.

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“…This approach successfully repolarized macrophages in the TME to an anti-tumor phenotype with minimal toxicity [222]. Recent work has also investigated the therapeutic potential of engineering nanoparticles derived from CCR2-overexpressing monocytes loaded with iron oxide to facilitate ferroptosis, repolarize local macrophage populations, and reduce metastatic burden [223]. Repolarization of macrophages from M2 to M1 was also achieved using self-assembled dual-inhibitor-loaded nanoparticles to target CSF-1 and Src homology 2 domain-containing phosphatase 2 pathways, which resulted in anti-tumor efficacy in mammary and melanoma pre-clinical mouse models [224].…”

Section: Repolarizationmentioning

confidence: 99%

Tissue-Resident and Recruited Macrophages in Primary Tumor and Metastatic Microenvironments: Potential Targets in Cancer Therapy

Cotechini

Atallah

Grossman

2021

Cells

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Macrophages within solid tumors and metastatic sites are heterogenous populations with different developmental origins and substantially contribute to tumor progression. A number of tumor-promoting phenotypes associated with both tumor- and metastasis-associated macrophages are similar to innate programs of embryonic-derived tissue-resident macrophages. In contrast to recruited macrophages originating from marrow precursors, tissue-resident macrophages are seeded before birth and function to coordinate tissue remodeling and maintain tissue integrity and homeostasis. Both recruited and tissue-resident macrophage populations contribute to tumor growth and metastasis and are important mediators of resistance to chemotherapy, radiation therapy, and immune checkpoint blockade. Thus, targeting various macrophage populations and their tumor-promoting phenotypes holds therapeutic promise. Here, we discuss various macrophage populations as regulators of tumor progression, immunity, and immunotherapy. We provide an overview of macrophage targeting strategies, including therapeutics designed to induce macrophage depletion, impair recruitment, and induce repolarization. We also provide a perspective on the therapeutic potential for macrophage-specific acquisition of trained immunity as an anti-cancer agent and discuss the therapeutic potential of exploiting macrophages and their traits to reduce tumor burden.

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Synergistic ferroptosis and macrophage re-polarization using engineering exosome-mimic M1 nanovesicles for cancer metastasis suppression

Cited by 34 publications

References 39 publications

Ferroptosis and Cancer: Complex Relationship and Potential Application of Exosomes

Ferroptosis and Cancer: Complex Relationship and Potential Application of Exosomes

M1 Macrophage-Derived Exosomes Loaded with Gemcitabine and Deferasirox against Chemoresistant Pancreatic Cancer

Tissue-Resident and Recruited Macrophages in Primary Tumor and Metastatic Microenvironments: Potential Targets in Cancer Therapy

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