Crosstalk between extracellular vesicles and tumor-associated macrophage in the tumor microenvironment

In concert with hijacking key genes to drive tumor progression, cancer cells also have the unique ability to dynamically interact with host microenvironment and discreetly manipulate the surrounding stroma, also known as the tumor microenvironment (TME), to provide optimal conditions for tumor cells to thrive and evade host immunity. Complex cellular crosstalk and molecular signaling between cancer cells, surrounding non-malignant cells, and non-cellular components are involved in this process. While intercellular communication traditionally centers around chemokines, cytokines, inflammatory mediators, and growth factors, emerging pathways involving extracellular vesicles (EVs) are gaining increasing attention. The immunosuppressive TME is created and maintained in part by the large abundance of tumor-associated macrophages (TMAs), which are associated with drug resistance, poor prognosis, and have emerged as potential targets for cancer immunotherapy. TMAs are highly dynamic, and can be polarized into either M1 or M2-like macrophages. EVs are efficient cell-cell communication molecules that have been catapulted to the center of TMA polarization. In this article, we pro-vide detailed examination of the determinative role of EVs in sustaining the TME through mediating crosstalk between tumor cells and tumor-associated macrophages.

Automated summary

In addition to hijacking key genes to drive tumor progression, cancer cells can dynamically interact with the host microenvironment and manipulate the surrounding stroma, known as the tumor microenvironment (TME), to create optimal conditions for tumor cells to thrive. This process involves complex cellular communication and molecular signaling, with emerging pathways involving extracellular vesicles (EVs) gaining attention.