z-logo
Premium
Interferon‐γ downregulates epidermal growth factor receptors on human melanoma cells
Author(s) -
Worm Margitta,
Makki Amira,
Dippel Edgar,
Czarnetzki Beate M.,
Schadendorf Dirk
Publication year - 1995
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.1995.tb00218.x
Subject(s) - epidermal growth factor , melanoma , cancer research , biology , cell culture , epidermal growth factor receptor , receptor , downregulation and upregulation , cytokine , cell growth , immunohistochemistry , interferon , interferon gamma , medicine , immunology , gene , biochemistry , genetics
Abstract Unregulated expression of epidermal growth factor receptor (EGF‐R) is a common event in neoplastic transformation and has been shown to be associated with melanocytic tumor progression. Modulation of such a receptor by pharmacological agents could therefore be of clinical interest. We have studied EGF‐R expression, its response to epidermal growth factor (EOF) and modulation effects by interferon gamma (IFNγ) on human melanoma cells. Addition of EOF, anti‐EGF and anti‐EGF‐R antibodies had no effect on proliferation of six melanoma cell lines tested. We report in this communication that EGF‐R expression on human melanoma cells can be modulated by IFNγ. In the melanoma cell lines treated with IFNγ. proliferative behavior was not affected; however, we demonstrate a downregulation of EGF‐R expression on the protein level, by immunohistochemistry and flow cytometric analysis, and an accumulation of EGF‐R mRNA by Northern blot analysis. The results suggest that IFNγ downregulates EGF‐R expression at a posttranscriptional level on human melanoma cells. This EGF/EGF‐R interaction and its modulation by IFNγ on human melanoma cells needs to be further clarified regarding its in vivo significance for the treatment and prognosis of malignant melanoma.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here