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Mechanism of Extracellular Vesicle Secretion Associated with TGF-β-Dependent Inflammatory Response in the Tumor Microenvironment

期刊

出版社

MDPI
DOI: 10.3390/ijms232315335

关键词

inflammation; angiogenesis; transforming growth factor beta; extracellular vesicles; tumor microenvironment

资金

  1. Individual Grants of Young Scientists (Nicolaus Copernicus University in Torun, Faculty of Medicine, Collegium Medicum in Bydgoszcz) [MN-IND.WL.6/2021]
  2. German Research Foundation (Deutsche Forschungsgemeinschaft [DFG]) [TR156/C05-246807620, SFB1009/B11-194468054, SFB1066/B06-213555243, SFB1450/C06-431460824]

向作者/读者索取更多资源

Extracellular vesicles play a central role in communication between tumor and non-tumor cells. The function of the endothelial barrier and the receptors on its surface are important for these interactions. Inflammation and dysregulation of TGF-beta signaling are associated with tumor progression. This review aims to explore the correlation between EV release, TGF-beta-dependent inflammation, and dysregulation of downstream TGF-beta signaling in cancer development.
Extracellular vesicles (EVs) serve as central mediators in communication between tumor and non-tumor cells. These interactions are largely dependent on the function of the endothelial barrier and the set of receptors present on its surface, as endothelial cells (ECs) are a plenteous source of EVs. The molecular basis for EV secretion and action in the tumor microenvironment (TME) has not been fully elucidated to date. Emerging evidence suggests a prominent role of inflammatory pathways in promoting tumor progression and metastasis. Although transforming growth factor beta (TGF-beta) is a cytokine with strong immunomodulatory and protective activity in benign and early-stage cancer cells, it plays a pro-tumorigenic role in advanced cancer cells, which is known as the TGF-beta paradox . Thus, the aim of this review is to describe the correlation between EV release, TGF-beta-dependent inflammation, and dysregulation of downstream TGF-beta signaling in the context of cancer development.

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