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J Cutan Pathol. 2007 Aug;34(8):606-11.

Signal transducer and activator of transcription-3 expression and activation is dysregulated in actinic cheilitis.

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  • 1Department of Microbiology and Immunology, São Leopoldo Mandic Dental Research Center, Rua Abolição, 1827 Ponte Preta, Campinas, São Paulo, CEP 13045-610 Brazil.



The present study evaluates the signal transducer and activator of transcription-3 (STAT-3) expression and activation in actinic cheilitis (AC) and the relationship of this protein with the degree of epithelial dysplasia.


Twenty-five cases of AC were analyzed. Normal lip mucosa was used as a control group. AC lesions were graded as mild, moderate and severe dysplasias. Immunohistochemistry for STAT-3 and phospho-STAT-3 (STAT-3P) was performed using the biotin-streptavidin-peroxidase method, and the sections were evaluated by three blinded examiners.


In normal lip mucosa, only cytoplasmic expression of STAT-3 was observed in the basal and parabasal layers. In AC, STAT-3 was expressed in the cell cytoplasm of the epithelial layers, except in the superficial layer. Nuclear expression of STAT-3 in occasional basal and parabasal cells was seen in moderate and severe dysplasias. In normal lip mucosa, nuclear expression of STAT-3P was found throughout the epithelium, except in the superficial layers, and it was more intense in the deeper layers. In AC, STAT-3P was also expressed in all layers, except for the superficial layer. However, in moderate and severe dysplasias, some epithelial cells exhibited loss of STAT-3P expression.


In AC, STAT-3 expression depends on the degree of dysplasia, and STAT-3 activation is dysregulated compared with normal tissue.

[PubMed - indexed for MEDLINE]
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