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Protein kinase C isoforms in normal and transformed cells of the melanocytic lineage

Selzer, E.*; Okamoto, I.; Lucas, T.; Kodym, R.; Pehamberger, H.; Jansen, B.

Original Articles

Enzymes belonging to the protein kinase C (PKC) family represent one of the major mediators of signal transduction in melanocytes. To identify PKC isoforms that may be associated with the process of malignant transformation and metastasis, we investigated the expression pattern of 11 different PKC isoforms (α, βI, βII, γ, δ, ∊, η, θ, ς, λ and ι) in melanoma lymph node metastases, in cell lines established from these metastases, in primary cell cultures from normal melanocytes, and in permanent cell lines established from spontaneously transformed melanocytes. PKC α, βI, βII, δ, ∊, η, ζ, λ and ι were found to be expressed in total lysates from melanoma metastases. In permanent cell lines established from these metastases, the expression levels of PKC βI, βII, δ, ∊ and η were lower or undetectable when compared with initial expression in tumour lysates. In normal primary melanocyte cultures, the PKC isoforms βII, δ, ∊, η and ι were undetectable. PKC γ and θ isoforms were undetectable in all melanocytic cell types examined. PKC ι was the only isoform exclusively detected in tumour lysates, in spontaneously transformed melanoma cells and melanoma cell lines, but not in normal melanocytes, and may therefore be associated with the transformed phenotype in human melanoma in vitro and in vivo.

Department of Radiotherapy and Radiobiology (E. Selzer, R. Kodym), Department of Clinical Pharmacology, Section of Experimental Oncology and Molecular Pharmacology (T. Lucas, B. Jansen), Department of Dermatology, Division of General Dermatology (I. Okamoto, H. Pehamberger, B. Jansen) and Ludwig Boltzmann Institute for Clinical and Experimental Oncology (H. Pehamberger), University Hospital Vienna, Währinger Gürtel 18-20, 1090 Vienna, Austria. Tel: (+43) 1 40400 7672; Fax: (+43) 1 40400 2666; Email:

(Received 29 April 2001; accepted in revised form 21 October 2001)

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© 2002 Lippincott Williams & Wilkins, Inc.