Abstract
Cancer can be described as a dynamic disease formed by malignant and stromal cells. The cellular interaction between these components in the tumor microenvironment (TME) dictates the development of the disease and can be mediated by extracellular vesicles secreted by tumor cells (TEVs). In this review, we summarize emerging findings about how TEVs modify important aspects of the disease like continuous tumor growth, induction of angiogenesis and metastasis establishment. We also discuss how these nanostructures can educate the immune infiltrating cells to generate an immunosuppressive environment that favors tumor progression. Furthermore, we offer our perspective on the path TEVs interfere in cancer treatment response and promote tumor recurrence, highlighting the need to understand the underlying mechanisms controlling TEVs secretion and cargo sorting. In addition, we discuss the clinical potential of TEVs as markers of cell state transitions including the acquisition of a treatment-resistant phenotype, and their potential as therapeutic targets for interventions such as the use of extracellular vesicle (EV) inhibitors to block their pro-tumoral activities. Some of the technical challenges for TEVs research and clinical use are also presented.
Highlights
Malignant tumors are defined as a microenvironment composed by different clones of tumor cells, and by stromal cells as well as extracellular matrix (ECM) (Quail and Joyce, 2013)
Remarkable progress has been made in the extracellular vesicle (EV) field, as summarized in Figure 2, there are some gaps in our understanding of molecular mechanisms that control vesicle packaging and how the cargo loading can be modified in response to different stimuli such as cancer therapies
This aspect is crucial for the comprehension of how EVs can promote resistance and tumor recurrence after therapy and to design new therapeutic strategies to minimize and block these pro-tumoral effects
Summary
Malignant tumors are defined as a microenvironment composed by different clones of tumor cells, and by stromal cells as well as extracellular matrix (ECM) (Quail and Joyce, 2013). All these components interact with each other dictating the natural history of the disease and the response to treatment. From an ecological point of view, these interactions can be described as cooperative or competitive and, in both cases, depend on the mechanism of cellular communication (Pelham et al, 2020) These interactions are dynamic and mediated by soluble factors secreted by cells or trapped in the ECM, and by extracellular vesicles (EVs) (Tkach and Théry, 2016)
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