Expressions of c-jun and p53 proteins in human middle ear cholesteatoma: relationship to keratinocyte proliferation, differentiation, and programmed cell death.

Abstract

The c-jun protein functions as a transcription factor for many genes, and the p53 protein functions as a negative regulator of cellular proliferation, which is related to the apoptosis pathway that induces DNA damage. It has recently been shown that c-jun promotes keratinocyte proliferation and p53 induces apoptosis of various cells. In this study, the presence of c-jun and p53 in cholesteatoma was demonstrated by immunoblotting assays using polyclonal rabbit anti-c-jun antibody and monoclonal anti-p53 protein antibody, respectively. The cholesteatoma tissue incubated with anti-c-jun antibody showed the staining of keratinocytes on the basal and spinous layers of epithelium. The c-jun protein was localized in the basal layer of normal skin, and the p53 protein was present in the nucleus of keratinocytes in the granular layer of cholesteatoma epithelium. The keratinocytes of normal external ear canal skins and normal human skins were slightly stained in the granular layer of the epidermis. The present findings suggest that c-jun and p53 proteins have a role in keratinocyte differentiation, proliferation, and apoptosis in the cholesteatoma.