Abstract
Cancer cells must adapt their metabolism in order to meet the energy requirements for cell proliferation, survival in nutrient-deprived environments, and dissemination. In particular, FA metabolism is emerging as a critical process for tumors. FA metabolism can be modulated through intrinsic changes in gene expression or signaling between tumor cells and also in response to signals from the surrounding microenvironment. Among these signals, extracellular vesicles (EVs) could play an important role in FA metabolism remodeling. In this review, we will present the role of EVs in tumor progression and especially in metabolic reprogramming. Particular attention will be granted to adipocytes. These cells, which are specialized in storing and releasing FAs, are able to shift tumor metabolism toward the use of FAs and, subsequently, increase tumor aggressiveness. Recent work demonstrates the involvement of EVs in this metabolic symbiosis.
Highlights
Cancer cells must adapt their metabolism in order to meet the energy requirements for cell proliferation, survival in nutrient-deprived environments, and dissemination
Our laboratory recently revealed that naïve adipocytes, which have never been in contact with tumor cells, secrete extracellular vesicle (EV) that promote melanoma aggressiveness through metabolic reprogramming in favor of FA oxidation (FAO) [89]
Among the metabolic pathways affected by EVs is FA metabolism
Summary
The communication between the cells found within tumors and their surrounding stroma can be mediated by soluble factors such as cytokines, chemokines, growth factors, and matrix remodeling enzymes [14]. The importance of EVs in this dialog is clearly recognized [11]. The importance of EVs in the communication between these cells is clearly recognized. Studies have proven the involvement of EVs in transfer of metastatic potential between tumor cells in vitro [19,20,21] and in vivo [22]. EVs can mediate drug resistance through the sequestration, transport, and/or expulsion of chemotherapeutic drugs from tumor cells [for recent reviews concerning this point, see [23, 24]]
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