SNAI2 promotes the malignant transformation of oral leukoplakia by modulating p‐EMT

Abstract Objective Snail family transcriptional repressor 2 (SNAI2) is a key regulator of partial epithelial‐mesenchymal transition (p‐EMT) and is associated with tumorigenesis. Whether SNAI2 promotes oral leukoplakia (OLK) malignant transformation by modulating p‐EMT is unclear. Materials and Methods This study utilized two clinical datasets (GSE26549 and GSE85195) from the Gene Expression Omnibus database, cytological experiments, and a 4‐nitroquinoline 1‐oxide‐induced mice model to explore the role of SNAI2 in OLK malignant transformation. Results The clinical cohort found SNAI2, as a risk factor (HR = 2.50, 95% CI: 1.08–5.79, p = 0.033), could promote OLK malignant transformation ( p = 0.012). Cytological experiments indicated that SNAI2 overexpression promoted DOK cell proliferation, invasion, migration, and increase the protein expression of p‐EMT relative signatures, whereas SNAI2 silencing has opposite effects. Furthermore, the mice model and clinical datasets demonstrated the expression of SNAI2 and p‐EMT relative signatures were increased with OLK malignant transformation. And SNAI2 was strongly correlated with p‐EMT. Besides, co‐expressed genes of SNAI2 were also enriched in p‐EMT relative biological processes and signaling pathways. Conclusions p‐EMT plays a significant role in promoting the OLK malignant transformation. As an important regulator of p‐EMT, SNAI2 could be a target to block the OLK malignant transformation.