Meis1 Negatively Regulates Epithelial-Mesenchymal Transition via Wnt/β-catenin Pathway in Oral Submucous Fibrosis

Oral submucous fibrosis (OSF) is an irreversible and potentially malignant oral disorder. Epithelial-mesenchymal transition (EMT) is a key driver of its pathogenesis. However, the underlying molecular mechanisms remain incompletely elucidated. This study aimed to investigate the role of Meis1, a novel regulatory molecule, in the pathogenesis of OSF and explore its underlying mechanism.

Bioinformatics analysis explored the correlation between Meis1 and OSF. Meis1 expression in clinical OSF tissues and cell models was verified by q-PCR, western blotting, and immunohistochemistry. Cell migration and proliferation were assessed via wound healing assays and EDU staining. RNA sequencing identified Meis1's downstream pathways. Rescue experiments determined if Meis1 regulates EMT via the Wnt/β-catenin pathway.

Meis1 was predicted and confirmed to be downregulated in OSF, with its expression showing a progressive decrease as the disease severity advanced. Meis1 overexpression reversed TGF-β1-induced EMT, while Meis1 knockdown activated the Wnt/β-catenin pathway. Notably, the EMT process induced by Meis1 knockdown was rescued by inhibition of the Wnt/β-catenin pathway.

This study identified Meis1 as a novel molecule involved in OSF progression. Furthermore, Meis1 suppressed EMT in OSF by inhibiting the Wnt/β-catenin pathway.

Our study might provide a novel potential target for the targeted therapy of OSF.