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

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.

Automated summary

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.