Oral‐specific ablation of <i>Klf4</i> disrupts epithelial terminal differentiation and increases premalignant lesions and carcinomas upon chemical carcinogenesis

Abstract

Klf4 ablation results in more severe dysplastic lesions in oral mucosa, with a tendency to higher incidence of SCC, after chemical carcinogenesis. We show here, in a context similar to the human carcinogenesis, that absence of Klf4 accelerates carcinogenesis and correlates with the absence of cytokeratin 1 expression. These results suggest a potential role for KLF4 as a tumor suppressor gene for the tongue epithelium.