Fig. 3

Different sources of EVs in the cancer-to-stroma communication network. Stromal cells are not bystanders in the development of tumors. a Cancer-associated fibroblast (CAF)-derived EVs loaded with TβRII and MFAP5, which reactivate the TGF-β signaling pathway, trigger the activation of MAPK and AKT signaling pathways and promote the proliferation and metastasis of OSCC. b Mesenchymal stem cell (MSC)-derived exosomal FGF-19 induces the EMT via the FGF-19/FGFR-4 signaling pathway and promotes tumor cell progression. c HPV and EBV can hijack cancer-derived EV production to regulate cell-to-cell communication and package onco-proteins or virus-coding miRNAs, such as E6/E7, MUC16, LMP1, EGFR, and miRNA-BART, which modulate the TME and promote tumor development. EVs from the saliva d and circulating blood e of patients with HNCs can be used not only as potential biomarkers to reflect the clinical stage of tumor pathology but also as carriers of active molecules involved in tumorigenesis