The evolving tumor microenvironment: From cancer initiation to metastatic outgrowth

Cancer Cell, Год журнала: 2023, Номер 41(3), С. 374 - 403

Опубликована: Март 1, 2023

Язык: Английский

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Comprehensive isolation of extracellular vesicles and nanoparticles

Nature Protocols, Год журнала: 2023, Номер 18(5), С. 1462 - 1487

Опубликована: Март 13, 2023

Язык: Английский

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Tumour extracellular vesicles and particles induce liver metabolic dysfunction

Nature, Год журнала: 2023, Номер 618(7964), С. 374 - 382

Опубликована: Май 24, 2023

Язык: Английский

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Extracellular vesicles and particles impact the systemic landscape of cancer

The EMBO Journal, Год журнала: 2022, Номер 41(18)

Опубликована: Сен. 2, 2022

Язык: Английский

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Pre-metastatic niche: formation, characteristics and therapeutic implication

Signal Transduction and Targeted Therapy, Год журнала: 2024, Номер 9(1)

Опубликована: Сен. 25, 2024

Язык: Английский

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Small Extracellular Vesicles From Infarcted and Failing Heart Accelerate Tumor Growth

Circulation, Год журнала: 2024, Номер 149(22), С. 1729 - 1748

Опубликована: Март 15, 2024

Myocardial infarction (MI) and heart failure are associated with an increased incidence of cancer. However, the mechanism is complex unclear. Here, we aimed to test our hypothesis that cardiac small extracellular vesicles (sEVs), particularly mesenchymal stromal cell-derived sEVs (cMSC-sEVs), contribute link between post-MI left ventricular dysfunction (LVD)

Язык: Английский

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Complement C3 of tumor-derived extracellular vesicles promotes metastasis of RCC via recruitment of immunosuppressive myeloid cells

Proceedings of the National Academy of Sciences, Год журнала: 2025, Номер 122(4)

Опубликована: Янв. 23, 2025

Heterogeneous roles of complement C3 have been implicated in tumor metastasis and are highly context dependent. However, the underlying mechanisms linking to remain elusive renal cell carcinoma (RCC). Here, we demonstrate that RCC cell-derived extracellular vesicles (EVs) contributes via polarizing tumor-associated macrophages (TAMs) into immunosuppressive phenotype recruiting polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs). Mechanistically, EV induces secretion CCL2 CXCL1 by lung subsequently enhances TAM polarization PMN-MDSC recruitment. Notably, targeting CCL2/CCR2 or CXCL1/CXCR2 axis with inhibitors RS504393 Navarixin, respectively, effectively suppresses induced RCC-derived a mouse model. Clinically, patients high expression poor prognosis. Collectively, our findings reveal tumor-derived an microenvironment TAMs, thus promoting metastasis.

Язык: Английский

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Contribution of tumor microenvironment (TME) to tumor apoptosis, angiogenesis, metastasis, and drug resistance

Medical Oncology, Год журнала: 2025, Номер 42(4)

Опубликована: Март 14, 2025

Язык: Английский

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The uptake of extracellular vesicles: research progress in cancer drug resistance and beyond

Drug Resistance Updates, Год журнала: 2025, Номер 79, С. 101209 - 101209

Опубликована: Фев. 1, 2025

Язык: Английский

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TGF-β induces cholesterol accumulation to regulate the secretion of tumor-derived extracellular vesicles

Journal of Experimental & Clinical Cancer Research, Год журнала: 2025, Номер 44(1)

Опубликована: Фев. 6, 2025

Abstract Background Cancer cells are avid extracellular vesicle (EV) producers. EVs transport transforming growth factor-β (TGF-β), which is commonly activated under late stages of cancer progression. Nevertheless, whether TGF-β signaling coordinates EV biogenesis a relevant topic that remains minimally explored. Method We sought after specific pathway mediators could regulate release. To this end, we used large number cell models, coupled to biological assays, unbiased proteomic and transcriptomic screens, followed by biology analyses, including drug resistance assays. Results report TGF-β, activating its type I receptor MEK-ERK1/2 signaling, increased the numbers released human cells. Upon examining cholesterol as mediator biogenesis, delineated whereby ERK1/2 acted phosphorylating sterol regulatory element-binding protein-2 transcriptionally induced 7-dehydrocholesterol reductase expression, thus raising abundance at both cellular levels. Notably, inhibition MEK or synthesis, impaired TGF-β-induced secretion, sensitized chemotherapeutic drugs. Furthermore, profiling two distinct populations revealed secreted TGF-β-stimulated were either depleted enriched for different sets cargo proteins. Among these, latent-TGF-β1 present in was not affected while pathway-related molecules (e.g., matrix metalloproteinases, MMP9) uniquely on strongly enhanced stimulation. EV-associated SMAD even when uptake blocked heparin, indicating competent capacity from target surface receptors. MMP inhibitor proteinase treatment EV-mediated suggesting require activity release active latent complex, function also linked transfer pro-migratory potential ability survive presence cytotoxic Conclusion Hence, novel cascade leads high rates generation response with being key intermediate step mechanism. Graphical • increases MEK-ERK1/2-SREBP2-DHCR7 transcriptional pathway. DHCR7 expression raises promotes carry MMP9 can activate recipient

Язык: Английский

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