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Differential Induction of Connexins 26 and 30 in Skin Tumors and Their Adjacent Epidermis

Nikolas K. Haass, Ewa Wladykowski, Sabine Kief, Ingrid Moll and Johanna M. Brandner

Department of Dermatology and Venerology, University Hospital Hamburg–Eppendorf, Hamburg, Germany

Correspondence and present address: Dr. Nikolas K. Haass, The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104. E-mail: nhaass{at}wistar.org

Gap junctions (GJs) have been shown to play a role in tumor progression including a variety of keratinocyte-derived and non-keratinocyte-derived skin tumors. Here we show that the synthesis of the GJ proteins connexin 26 and connexin 30 (Cx26 and Cx30) is induced in keratinocyte-derived epithelial skin tumors whereas there is either no change or a downregulation of Cx43. Cx26, Cx30, and Cx43 are absent in non-epithelial skin tumors. Further, Cx26 and Cx30 are induced in the epidermis adjacent to malignant melanoma but absent in the epidermis adjacent to benign non-epithelial skin lesions (melanocytic nevi and angioma). The keratinocyte-derived skin tumors are very heterogeneous regarding the Cx26/Cx30 pattern in the epidermis at the periphery of the tumors. We did not observe any difference in the localization of the very similar proteins Cx26 and Cx30 but a variation in intensity of immunoreactivity. As the staining patterns of Cx26 and Cx30 antibodies are not identical to those of CK6, a marker for hyperproliferation, and CK17, a marker for trauma, we discuss that the induction of these gap junctional proteins exceeds a reflection of reactive hyperproliferative or traumatized epidermis. We further discuss the putative roles of these gap junctional proteins in tumor progression. (J Histochem Cytochem 54:171–182, 2006)

Key Words: gap junction • skin cancer • melanoma • nevus • basal cell carcinoma • squamous cell carcinoma • cell–cell communication

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