口腔癌细胞来源外泌体miR-582-3p通过靶向SFRP1驱动口腔癌细胞的恶性表型OACSTPCD

Objective:To explore the supportive effects of exosomal microRNA-582-3p(miR-582-3p)on the malig-nant behaviors of oral cancer cells and its potential mechanism.Methods:Oral cancer serum and cell media were collected for exosome isolation.Transmission electron microscopy and nanoparticle tracking analysis were performed for exosome identi-fication and concentration and diameters measurement.miR-582-3p level and secreted frizzled-related protein 1(SFRP1)mRNA expression were detected by quantitative real-time PCR.Oral cancer cell viability,proliferation,migration,and inva-sion were assessed by cell count kit-8(CCK-8),EdU,colony formation,wound healing,and Transwell assays.The direct inter-action between miR-582-3p and SFRP1 was determined by dual-luciferase activity assay.Western blot analysis was performed to detect exosome-related proteins,including HSP70,CD81,CD9,CD63,TSG101 and Alix,as well as SFRP1 protein expres-sion levels.A xenograft experiment was utilized to confirm the tumor-promoting role of exosomal miR-582-3p in oral cancer.Results:miR-582-3p was highly expressed in oral cancer tissues,serum,cells and exosomes derived from serum and cells.O-ral cancer cell-derived exosomal miR-582-3p significantly promoted the viability,proliferation,migration,and invasion of oral cancer cells.Dual-luciferase reporter assay revealed that miR-582-3p can directly bind to the 3′-UTR of SFRP1 and inhibit its expression.Restoration of SFRP1 expression rescued the malignant phenotypes induced by exosomal miR-582-3p.In addi-tion,enforced expression of miR-582-3p facilitated oral cancer growth in a xenograft model,accompanied by downregulation of SFRP1.Conclusion:Oral cancer cell-derived exosomal miR-582-3p promotes the malignant behaviors of oral cancer cells by targeting SFRP1.