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Overexpression of protein kinase C-α and -β isozymes by stromal dendritic cells in basal and squamous cell carcinoma

Lookup NU author(s): Professor Nick ReynoldsORCiD, Carole Todd, Dr Brian Angus

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Abstract

Protein kinase C (PKC) isozymes transduce signals from cell surface receptors and thereby regulate important cellular functions in skin including keratinocyte growth and differentiation. Overexpression of individual PKC isozymes results in aberrant cell growth and in certain instances tumorigenicity. PKC is implicated in tumour promotion in mouse skin. Abnormal expression of PKC has been reported in several human cancers. We have, therefore, investigated expression of PKC-α and -β in basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) by immunohistochemistry. Sections were stained with specific antibodies to PKC-α, PKC-β, CD1a, T cells, B cells and dermal dendritic cells (factor XIIIa), using an immunoperoxidase technique. PKC-α and PKC-β were not detected in tumour cells in BCCs or SCCs. In SCCs, PKC-β immunostaining revealed positively stained inflammatory and dendritic cells scattered through the stroma: PKC-α immunostaining was essentially negative. In contrast, in BCCs, PKC-α and PKC-β+ dendritic and spindle-shaped cells were observed in the stroma, immediately adjacent to the tumour islands. Double-labelling experiments showed that a proportion (approximately 20%) of PKC-β+ dendritic cells also expressed factor XIIIa. BCCs depend on stroma for growth: PKC regulates expression of type IV collagenase and stromelysin III and interactions between tumour and stroma may be important in determining tumour invasion and metastasis. Therefore, overexpression of PKC-α and -β by stromal dendritic cells in BCCs suggests that PKC activation may be involved in stromal/tumour interactions in these tumours.


Publication metadata

Author(s): Reynolds NJ, Todd C, Angus B

Publication type: Article

Publication status: Published

Journal: British Journal of Dermatology

Year: 1997

Volume: 136

Issue: 5

Pages: 666-673

Print publication date: 01/05/1997

ISSN (print): 0007-0963

ISSN (electronic): 1365-2133

Publisher: Wiley-Blackwell

URL: http://dx.doi.org/10.1046/j.1365-2133.1997.6531617.x

DOI: 10.1046/j.1365-2133.1997.6531617.x

PubMed id: 9205496


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