The Journal of Clinical Endocrinology & Metabolism · 1986 · 23 citations · 28 references
Life SciencesCancer BiologyCell BiologyCell SignalingEndocytosisSignal TransductionCancer Cell SignalingCell-surface ReceptorsEndometrial CancerGrowth Factor SignalingReceptor-mediated EndocytosisEpidermal Growth Factor Receptor EndocytosisEpidermal Growth Factor Receptor InhibitionEpidermal Growth Factor Receptor SignalingLigand InternalizationLigand-induced InternalizationMorphological Changes During GrowthScatchard AnalysisSurface Receptor Binding
Specific epidermal growth factor (EGF) receptors were measured in RL95-2 human endometrial carcinoma cells. At 37 C, binding of 125I-labeled EGF was associated with marked ligand internalization. Maximal cell surface binding occurred within 10 min. Bound [125I]EGF was partially degraded to low mol wt products, and this degradation was blocked by the lysosomotropic compound ammonium chloride. At 4 C, maximal cell surface binding occurred at 3 h. Scatchard analysis of data obtained after 3 h at 4 C revealed a single order of binding sites with a Kd of 1.8 nM and approximately 150,000 surface receptors/cell. EGF, at a concentration of 0.83 nM, inhibited the proliferation of RL95-2 cells. Inhibition was reversible and was associated with morphological changes leading to a fusiform appearance of the growth-arrested cells. These findings indicate that RL95-2 human endometrial carcinoma cells bind, internalize, and degrade EGF in a manner similar to that described for other target cells for EGF action. The ability of EGF to inhibit the growth of RL95-2 cells supports the hypothesis that this type of inhibition is dependent on postreceptor events, rather than on the presence of an overabundance of EGF receptors.
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Tomoyuki Kawamoto, Jun Sato, Anh D. Le et al. · Proceedings of the National Academy of Sciences · 1983 · 796 citations · Full text