Characterization and mutual ligand-induced modulation of epidermal growth factor and interferon-alpha receptors on renal carcinoma cells in vitro

• Published in: Anti-cancer drugs Vol. 6; no. 5; p. 686
• Main Authors: Heise, H, Depenbrock, H, Rastetter, J W, Hanauske, A R
• Format: Journal Article
• Language: English
• Published: England 01.10.1995
• Subjects: Adenocarcinoma - drug therapy; Adenocarcinoma - metabolism; Adenocarcinoma - pathology; Binding, Competitive; Carcinoma - drug therapy; Carcinoma - metabolism; Carcinoma - pathology; ErbB Receptors - drug effects; ErbB Receptors - metabolism; Humans; Kidney Neoplasms - drug therapy; Kidney Neoplasms - metabolism; Kidney Neoplasms - pathology; Receptor, Interferon alpha-beta; Receptors, Interferon - metabolism; Tumor Cells, Cultured
• ISSN: 0959-4973
• DOI: 10.1097/00001813-199510000-00008

We have determined the binding of epidermal growth factor (EGF) and interferon (IFN)-alpha to their specific receptors on four renal carcinoma cell lines. CaKi-2, a-498 and ACHN cell lines express high numbers, and CaKi-1 expresses low number of EGF receptors (EGFRs). On all four renal carcinoma cell lines, we have also detected specific IFN-alpha binding sites. EGF and IFN-alpha binding to their receptors caused modulation of the other ligand's receptor binding. Scatchard analyses of binding data showed that IFN-alpha treatment leads to an increase of EGFR number in three out of four cell lines and to a decrease of EGFR number in one out of four (CaKi-1). No significant changes in EGF binding affinities were detected. EGF induced a reduction in IFN-alpha receptor number in all four cell lines without significant changes in IFN-alpha binding affinities. We hypothesize that presence of EGF in the microenvironment of renal cancer cells may modulate the biological effects of IFN and consequently decrease its antiproliferative activity.