PMID: 6979383Jul 1, 1982Paper

Cell cycle variation in 125I-labeled epidermal growth factor binding in chemically transformed cells

Cancer Research
R A RobinsonH L Moses

Abstract

Previous studies have shown that the nontransformed AKR-2B cells when arrested in the G1 phase of the cell cycle due to low-molecule-weight nutrient (amino acid) deficiency exhibit a 5- to 10-fold lower level of epidermal growth factor (EGF) receptor activity than do the same cells in the rapidly growing state or arrested in G1 due to growth factor deficiency. The chemically transformed AKR-MCA and C3H/MCA-58 cell lines spontaneously arrest growth in G1 due to nutrient deficiency when grown to saturation density in medium with 10% fetal bovine serum. An examination of 125I-labeled EGF binding in rapidly growing and G1-arrested AKR-MCA and C3H/MCA-58 cells showed that the G1-arrested chemically transformed cells also have a 10- to 20-fold reduction in the amount of 125I-labeled EGF binding relative to the same cells in the rapidly growing state. Stimulation of DNA synthesis in the arrested cells by the addition of serum-free medium caused a 6- to 10-fold increase in 125I-labeled EGF binding. This recovery of receptor activity was inhibited by actinomycin D and cycloheximide, suggesting that new messenger RNA synthesis as well as increased protein synthesis is necessary for the recovery of EGF binding. A comparison of EGF binding...Continue Reading

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