The tumor microenvironment (TME) contains non-cancerous host cells, including endothelial cells, fibroblasts, adipocytes, neurons, adaptive immune cells, and innate immune cells, and components presented in the tumor, including the extracellular matrix (ECM) and molecules produced and released by them, like chemokines, growth factors, cytokines, and extracellular vesicles.
The TME is closely involved in the genesis and progression of cancers, in which tumor cells are harbored and interact with surrounding cells via the lymphatic and circulatory systems, while normal cells in the TME also play critical roles in all the phases of tumorigenesis by triggering and promoting abnormal cell proliferation.
Fig.1 Schematic overview of important mechanisms and interactions of the TME.1
The evolution and dynamic balance of the TME are modulated by interactions in and across malignant, stromal, endothelial, and immune cells, which often involve extracellular metabolites, composing a source of energy supply and acting as signals between different cellular compartments.
Compared with targeting tumor cells directly, there is a significant advantage in regarding the TME as a therapeutic target, since tumor cells are prone to drug resistance because of genomic instability, while non-cancerous cells in the TME are more stable in genomics and more vulnerable to therapy. Therefore, the TME as a therapeutic target in cancer has attracted intensive attention for research and clinical purposes.
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