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Cathepsin K expression in basal cell carcinoma
Author(s) -
Ishida M.,
Kojima F.,
Okabe H.
Publication year - 2013
Publication title -
journal of the european academy of dermatology and venereology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.655
H-Index - 107
eISSN - 1468-3083
pISSN - 0926-9959
DOI - 10.1111/j.1468-3083.2011.04436.x
Subject(s) - actinic keratosis , basal cell carcinoma , pathology , stromal cell , cathepsin d , cathepsin , medicine , immunohistochemistry , cathepsin b , cancer research , biology , basal cell , enzyme , biochemistry
Background Cathepsin K is a cysteine protease with strong collagenolytic and elastolytic properties. Recently, cathepsin K expression in tumour cells of malignant melanoma and in the stromal cells of squamous cell carcinoma of the skin has been reported to play an important role in tumour progression. However, its expression profile in basal cell carcinoma (BCC) has not yet been clarified. Objective The aim of this study is to examine the expression profile of cathepsin K in both the tumour cells and the peritumoural stromal cells of BCC in comparison with its expression in normal skin. Methods Fifty consecutive operative cases of BCC, 10 cases of actinic keratosis, 10 cases of Bowen’s disease and five normal skin tissues were assessed for cathepsin K expression by immunohistochemical methods. Results In normal skin, cathepsin K expression was observed in the stratum corneum, mature sebaceous cells and outer root sheath of the hair follicles. Cathepsin K was expressed in the tumour cells of all BCC cases, in which 90% showed diffuse expression (>51% of tumour cells), as well as in the peritumoural stromal cells in all BCC cases. Focal cathepsin K expression was observed in the tumour cells of Bowen’s disease (2/10 cases), but not in any of actinic keratosis (0/10 cases). Conclusion Cathepsin K expression may contribute to tumour invasion and peculiar histopathological features, such as fibromucinous stroma around the tumour nests by mediating extracellular matrix degradation in BCC.