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Cell Cycle Variation in ¹²⁵I-labeled Epidermal Growth Factor Binding in Chemically Transformed Cells¹

Departments of Cell Biology [R. A. R., E. L. B., M. E. V., H. L. M.] and Pathology [R. A. R., H. L. M.], Mayo Clinic, Foundation and Medical School, Rochester, Minnesota 55905

Previous studies have shown that the nontransformed AKR-2B cells when arrested in the G₁ phase of the cell cycle due to low-molecular-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 in C3H/MCA-58 cells and the nontransformed parent line (C3H/10T) in the rapidly growing state showed the same approximate level of receptor activity. However, the rapidly growing AKR-MCA cells had approximately one-tenth the amount of EGF binding as did the rapidly growing nontransformed parent line (AKR-2B). Scatchard analysis of binding data showed a 10-fold greater number of receptors in the AKR-2B cells relative to the AKR-MCA cells with a lesser difference in apparent receptor affinity. The chemically transformed BP-3T3, like the other two chemically transformed lines, was also demonstrated to arrest growth spontaneously due to nutrient deficiency with an associated 100-fold decrease in EGF binding. Rapidly growing BP-3T3 cells had only slightly less ¹²⁵I-labeled EGF binding than did the nontransformed parent line (BALB-3T3) in the rapidly growing state. The data indicate that one mechanism for reduction of EGF binding in chemically transformed cells is the propensity of these cells to arrest growth in G₁ at saturation density due to low-molecular-weight nutrient deficiency, a state associated with decreased EGF binding.

¹ Supported by USPHS Grant CA 27217 awarded by the National Cancer Institute, Department of Health and Human Services.

² To whom requests for reprints should be addressed.

Received 1/ 4/82. Accepted 3/30/82.