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

被引:5
|
作者
Curyl, Patricia R.
Furuse, Cristiane
de Araujo, Ney S.
de Araujo, Vera C.
机构
[1] Sao Leopoldo Mandic Dental Res Ctr, Dept Oral Pathol, BR-13045610 Campinas, SP, Brazil
[2] Sao Leopoldo Mandic Dental Res Ctr, Dept Microbiol & Immunol, Campinas, SP, Brazil
[3] Univ Sao Paulo, Sch Dent, Dept Oral Pathol, Campinas, SP, Brazil
关键词
D O I
10.1111/j.1600-0560.2006.00668.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
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.
引用
收藏
页码:606 / 611
页数:6
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