RESUMO
BACKGROUND: The expression of N-ras and ets-1 proteins was investigated in an experimental model of chemically-induced carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats. MATERIALS AND METHODS: Tissue sections ranging from normal mucosa to moderately-differentiated oral squamous cell carcinoma were studied using monoclonal antibodies against N-ras and ets-1 proteins. RESULTS: In diabetic rats, N-ras expression increased with tumor advancement, while in normal rats N-ras was not detected in initial stages of oral oncogenesis and increased only in well-differentiated OSCC. The same pattern of elevated ets-1 expression was observed both in diabetic and normal rats, but in cancerous stages this expression was higher in diabetic than in normal rats. CONCLUSION: It seems that diabetes may contribute to increased cell proliferation due to N-ras constitutive activation, as well as to enhanced invasion and metastatic potential by increasing ets-1 levels.
Assuntos
Carcinoma de Células Escamosas/secundário , Diabetes Mellitus Tipo 1/metabolismo , Neoplasias Bucais/patologia , Proteína Proto-Oncogênica c-ets-1/metabolismo , Proteínas ras/metabolismo , Animais , Anticorpos Monoclonais , Biópsia , Carcinoma de Células Escamosas/complicações , Carcinoma de Células Escamosas/metabolismo , Divisão Celular/fisiologia , Diabetes Mellitus Tipo 1/complicações , Modelos Animais de Doenças , Feminino , Imuno-Histoquímica , Neoplasias Bucais/complicações , Neoplasias Bucais/metabolismo , Lesões Pré-Cancerosas/complicações , Lesões Pré-Cancerosas/metabolismo , Lesões Pré-Cancerosas/patologia , Proteína Proto-Oncogênica c-ets-1/imunologia , Ratos , Ratos Sprague-Dawley , Proteínas ras/imunologiaRESUMO
BACKGROUND: The expression of tumour suppressor p53 and oncogene c-myc was investigated in an experimental model of chemically induced carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats. MATERIALS AND METHODS: Tissue sections ranging from normal mucosa to moderately differentiated oral squamous cell carcinoma were studied using monoclonal antibodies against mutant p53 and c-myc proteins. RESULTS: From hyperplasia to later stages of oral oncogenesis, mutant p53 expression was at higher levels in diabetic rats in comparison to normal animals, although the pattern of expression was similar. In contrast, c-myc expression was significantly higher in diabetic than in normal rats only in normal mucosa and hyperplasia. CONCLUSION: It seems that diabetes contributed to increased accumulation of mutations in the p53 gene, contributing to increased proliferation of tumour cells during oral oncogenesis. Additionally, diabetes appeared to enhance c-myc expression only in the initial stages of oral oncogenesis.
