TABLE 4.

The role of exosomes in metabolism reprogramming.

Phenotype	Type of primary cancer	Contents in exosomes	Target organ	Specific mechanism	References
Metabolism reprogramming	Breast cancer	miR-122	lung fibroblasts and brain astrocytes	Downregulating the PKM2 and GLUT1 and glucose uptake in niche cells; increasing glucose availability in cancer cells	Fong et al. (2015)
	Breast cancer	miR-105	CAFs	If nutrients are sufficient, the reprogrammed CAFs fuel adjacent cancer cells by enhancing glucose and glutamine metabolism; If not, the reprogrammed CAFs convert metabolic wastes into energy-rich metabolites	Yan et al. (2018)
	Breast cancer	miR-105, miR-204	Fibroblasts	Targeting RAGC to regulate mTORC1 signaling and alter the spectrum of de novo protein synthesis in fibroblasts.	Fong et al. (2021)
	Nasopharyngeal carcinoma	LMP1	CAFs	Aerobic glycolysis and autophagy in activated CAFs increasing energy-rich nutrients (lactate and β-HB) to “feed” cancer cells	Wu et al. (2020)
	Melanoma	miR-155, miR-210	Fibroblasts	Increasing aerobic glycolysis and decreasing oxidative phosphorylation in fibroblasts to favor PMN formation	Shu et al. (2018)
	Prostate cancer	CAFs-derived exosomes	Cancer cells	Under nutrient deprivation or nutrient stressed conditions, CAFs-derived exosomes inhibiting mitochondrial oxidative phosphorylation and increasing glycolysis and glutamine-dependent reductive carboxylation in cancer cells	Zhao et al. (2016)

Abbreviation: PKM2, glycolytic enzyme pyruvate kinase; CAFs, cancer-associated fibroblasts; RAGC, a component of Rag GTPases; LMP1, membrane protein 1; β-HB, lactate and β-hydroxybutyrate; PMN, pre-metastatic niche.