Objective To investigate the role and mechanism of PD-L1 in oral cancer metastasis based on TCGA and GEO databases. Methods The expression characteristics and clinical significance of PD-L1 in oral cancer were analyzed using the TCGA database. qRT-PCR was used to detect PD-L1 expression levels in different oral cancer cell lines. The effects of PD-L1 knockdown on the proliferation, migration, and invasion of oral cancer cells (CAL27 and SCC25) were evaluated via CCK-8 assay, wound healing assay, Transwell assay and Matrix gel invasion experiment. The interaction network between PD-L1 and functional genes of oral cancer patients was constructed by using STRING software and GEO database, and key pathways were screened through KEGG enrichment analysis. qRT-PCR was employed to validate the regulatory relationship between PD-L1 and key genes. Results TCGA data revealed that PD-L1 was highly expressed in oral cancer patients and correlated with lymph node metastasis. PD-L1 was also highly expressed in oral cancer cell lines. PD-L1 knockdown significantly inhibited the proliferation, migration, and invasion of Cal27 and SCC25 cells. KEGG analysis indicated that PD-L1 activates the JAK/STAT pathway by upregulating CXCL9 and CXCL10, thereby promoting STAT1 expression to regulate oral cancer metastasis. Inhibition of the JAK/STAT pathway further suppressed the proliferation, migration, invasion, and expression of STAT1, CXCL9, and CXCL10 in Cal27 and SCC25 cells. Conclusions PD-L1 may promote oral cancer cell proliferation, migration, and invasion by upregulating CXCL9 and CXCL10 to regulate the JAK/STAT pathway and enhance STAT1 expression, ultimately driving oral cancer growth and metastasis.