Abstract
Exosomes, the smallest group of extracellular vesicles, carry proteins, miRNA, mRNA, DNA, and lipids, which they efficiently deliver to recipient cells, generating a communication network. Exosomes strongly contribute to the immune suppressive tumor microenvironment of head and neck squamous cell carcinomas (HNSCC). Isolation of exosomes from HNSCC cell culture or patient’s plasma allows for analyzing their molecular cargo and functional role in immune suppression and tumor progression. Immune affinity-based separation of different exosome subsets, such as tumor-derived or T cell-derived exosomes, from patient’s plasma simultaneously informs about tumor status and immune dysfunction. In this review, we discuss the recent understanding of how exosomes behave in the HNSCC tumor microenvironment and why they are promising liquid biomarkers for diagnosis, prognosis, and therapy in HNSCC.
Highlights
Head and neck squamous cell carcinomas (HNSCC) account for the sixth most common cancer worldwide and are characterized by profound immune suppression
Similar studies revealed that miR-21 in serum-derived exosomes correlated with advanced tumor stage and metastasis in laryngeal (LSCC) [70] and esophageal squamous cell carcinoma (ESCC) [71]
Proteins clustered in pathways related to tumorigenesis and angiogenesis pathways. These findings suggest that the content of circulating plasma-derived exosomes has a relevant function in the treatment response of HNSCC patients
Summary
Head and neck squamous cell carcinomas (HNSCC) account for the sixth most common cancer worldwide and are characterized by profound immune suppression. Oral squamous cell carcinoma (OSCC)-derived exosomes carrying EGFR transformed normal epithelial cells into a mesenchymal phenotype, and the anti-EGFR therapeutic antibody cetuximab inhibited this carcinogenic effect of TEX [39]. TEX derived from hypoxic OSCC cells promoted migration and invasion of normoxic OSCC cells by delivery of miR-21 [42] Overall, these observations emphasize that TEX-mediated modulation of the TME contributes to immune suppression, tumor growth, and metastasis in HNSCC. Studies with xenograft tumor models showed that OSCC cell-derived exosomes promoted tumor growth in vivo [43]. TEX administration resulted in increased vascularization within the tumor and promoted angiogenesis in 4NQO-conditioned mice [37] HPV(+) UM-SCC-2, UM-SCC-47, UPCI-SCC-90, HPV(−) PCI-13, and PCI-30 HNSCC cell lines HPV(+) UM-SCC-2, UM-SCC-47, UPCI-SCC-90, HPV(−) PCI-13, and PCI-30 HNSCC cell lines HPV(+) SCC-90, SCC-47, SCC-104, HPV(−) SAS, CAL-27, and CAL-33
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