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Signal transducer and activator of transcription‐3 expression and activation is dysregulated in actinic cheilitis
Author(s) -
Cury Patricia R.,
Furuse Cristiane,
De Araújo Ney S.,
De Araújo Vera C.
Publication year - 2007
Publication title -
journal of cutaneous pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 75
eISSN - 1600-0560
pISSN - 0303-6987
DOI - 10.1111/j.1600-0560.2006.00668.x
Subject(s) - stat , stat protein , immunohistochemistry , pathology , epithelial dysplasia , dysplasia , cytoplasm , activator (genetics) , basal (medicine) , biology , medicine , signal transduction , microbiology and biotechnology , stat3 , receptor , insulin
Background:  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. Methods:  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. Results:  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. Conclusion:  In AC, STAT‐3 expression depends on the degree of dysplasia, and STAT‐3 activation is dysregulated compared with normal tissue.

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