Epidermal growth factor inhibits the proliferation of a human endometrial carcinoma cell line

Murray Korc, J. Padilla, D. Grosso

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

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 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 K(d) 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.

Original languageEnglish (US)
Pages (from-to)874-880
Number of pages7
JournalJournal of Clinical Endocrinology and Metabolism
Volume62
Issue number5
StatePublished - 1986
Externally publishedYes

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Endometrial Neoplasms
Epidermal Growth Factor
Cells
Cell Line
Ammonium Chloride
Cell Surface Receptors
Cell growth
Growth
Binding Sites
Ligands
Degradation

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Epidermal growth factor inhibits the proliferation of a human endometrial carcinoma cell line. / Korc, Murray; Padilla, J.; Grosso, D.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 62, No. 5, 1986, p. 874-880.

Research output: Contribution to journalArticle

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