Exosomes-Transferred Socs3 Inhibits DCS Activity In OSCC

This study aims to figure out the role of SOCS3 in OSCC progression and investigate its potential regulatory mechanisms on dendritic cells, which are responsible for initiating and modulating adaptive immune responses. Bioinformatics analyses were conducted to assess SOCS3 expression in HNSCC and its effect on the immune microenvironment. SOCS3 expression levels in OSCC cells were then detected using qRT-PCR and Western blot. Wound healing, CCK-8 proliferation, apoptosis, and Transwell migration assays were performed to explore the role of SOCS3 in OSCC progression. Immunofluorescence staining was utilized to determine the subcellular localization of SOCS3. Ultracentrifugation was used to extract OSCC-derived exosomes and these exosomes were labeled with PKH67 fluorescent dye and observed via confocal microscopy. Flow cytometry was used to assess the impact of OSCC-derived SOCS3 on DC maturation. Finally, RNA-seq and the construction of in vitro cell models were performed to explore the potential mechanisms of the effect of OSCC exosome-derived SOCS3 on DC activity. SOCS3 expression in OSCC cells is increased. SOCS3 scatterring in the cytosol can be released extracellularly through the exosome pathway and captured by DCs. Regulating the CSF2/CXCL5-related IL-17 signaling pathway to inhibit the activity of DCs may account for the reduced 5-year survival rate in OSCC patients with high SOCS3 expression. Our study elucidates the role and potential mechanisms of SOCS3 in regulating the tumor microenvironment of OSCC via exosomes, which provides a theoretical basis for developing new targeted and immunotherapeutic strategies for OSCC.