Increased risk of oral cancer in diabetic animals is not associated with c-jun activation pathway

Summary Purpose The expression of oncogenic protein c-jun was investigated in an experimental model of chemically induced carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats. Material and methods Thirteen diabetic and twelve normal rats developed cancer after 4-nitroquinoline- N -oxide treatment, while six diabetic and six normal animals were used as controls. The biopsies were classified pathologically from oral mucosal dysplasia to moderately differentiated oral squamous cell carcinoma (OSCC) and studied immunohistochemically using monoclonal antibody against c-jun protein. Results Higher c-jun levels were observed in non-cancerous and precancerous stages of normal rats compared with diabetic rats, while in different tumour stages, the expression of c-jun was practically identical for both groups. Conclusion It seems that diabetes does not affect the c-jun N-terminal kinase (JNK)/c-jun pathway.