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Figure 1. Overview of the metabolic alterations on cancer cell lines and tumors promoted by EVs derived from macrophages, fibroblasts, adipocytes, and AT. Fibroblasts liberate exosomes-containing lncRNA SNHG3, leading to positive regulation of PKM, resulting in the augmentation of glycolysis carboxylation and reduction of mitochondrial OXPHOS in breast cancer cell lines. Prostate cancer cells stimulated with CDEs demonstrated increased glucose uptake, glycolysis, lactate secretion, reductive carboxylation of glutamine, and reduced OXPHOS. These effects were possibly achieved by miR-22, miR-let7a, and miR-125b interaction through CDE delivery. CDEs transport LINC01614 to lung cancer cell lines, upregulating OXPHOS, glutamine transporters, and ATP synthesis. CDEs carrying lower concentrations of miR-7641 promote HIF-1α stabilization, resulting in an upregulation of HK2, GLUT1, LDHA, and increased glycolysis rate and cell proliferation in breast cancer cell lines. TAM-EVs deliver HISLA to breast cancer cells, generating enhanced glucose consumption, lactate production, ¹⁸FDG accumulation, and elevated GLUT1, GLUT3, HK2, and HIF-1α expression. DOCK 7 was found to be carried on the surface of TAM-EVs, leading to increased cholesterol content and altered cholesterol metabolism in CRC cells. TAM-derived exosomes demonstrated a positive regulation of glucose consumption, lactate production, and GLUT1, LDHA, and HK2 expression in HCC. This effect was due to the transport of lncMMPA by TAM-derived exosomes. Moreover, TAM-derived exosomes were observed to carry miR-193-3b-3p, culminating in enhanced glutamine uptake in the human pancreatic adenocarcinoma cell line. AD-EXOs promote ferroptosis resistance mediated by the transference of MTTP to colorectal cancer cell lines, affecting the response to chemotherapy. The miRNAs miR-155-5p, miR-10a-3p, and miR-30a-3p were proposed to be enriched in O-EVs and delivered to human breast cancer cell lines, stimulating increased mitochondrial density, oxygen consumption rate, and ATP production. AD EVs carry enzymes responsible for FAO, upregulating this pathway, leading to an increased invasion and migration of the human melanoma cell line. AD EVs increase glucose uptake, lactate production, and ATP generation in prostate cancer cell lines, although the EVs cargo is unknown. EVs: Extracellular vesicles; AT: adipose tissue; SNHG3: small nucleolar RNA host gene 3; HIF-1α: hypoxia-inducible factor 1-alpha; DOCK 7: dedicator of cytokinesis 7; TAMs:tumor-associated macrophages; CRC:colorectal cancer; HCC:hepatocellular carcinoma; lncRNA: long non-coding RNA; lncMMPA: lncMMPA: RP-11-1100L38; ATP: adenosine triphosphate; FAO: fatty acid oxidation; ¹⁸FDG accum.: ¹⁸F-fluorodeoxyglucose accumulation; Glutamine carb.: Glutamine carboxylation; Glucose cons.: Glucose consumption; GLUT: glucose transporter; Glucose up.: Glucose uptake; HK2: hexokinase 2; LDHA exp.: lactate dehydrogenase expression; Lactate prod.: Lactate production; Lactate sec.: Lactate secretion; lnc-RNA: long non-coding ribonucleic acid; miR: micro-RNA; MTTP: microsomal triglyceride transfer protein; OXPHOS: oxidative phosphorylation; Oxygen cons. rate: Oxygen consumption rate; PKM exp.: pyruvate kinase M expression (Created with BioRender).