Expression of β-catenin in rat oral epithelial dysplasia induced by 4-nitroquinoline 1-oxide

The aim of this study was to evaluate whether β-catenin accumulation is useful for diagnosing the malignant potential of oral precancerous lesions. We investigated oral epithelial dysplasia adjacent to early cancer induced by 4-nitroquinoline 1-oxide in rats. Localization of β-catenin and cell proliferation were detected immunohistochemically, and exon 3 of the β-catenin gene was analyzed. Accumulation of β-catenin in the cytoplasm and nucleus was evident in 10 of 16 dysplasia lesions. Since almost all of the dysplastic lesions in these rats transformed to invasive cancer, β-catenin accumulation may contribute to the early stage of carcinogenesis. The Ki-67 labeling index was significantly higher in dysplasia and early cancer than in no change. However, there were no significant differences between the expression patterns of β-catenin protein, suggesting that other proliferation pathways are involved in the early stage of tumor development in addition to β-catenin accumulation. No mutations of exon 3 of the β-catenin gene were detected in any of the dysplasia or early cancer lesions. These findings suggested that β-catenin accumulation in the cytoplasm and nucleus without mutation of exon 3 is an early event during carcinogenesis in this tongue cancer model.