Treatment of the transformed mouse embryo fibroblast cell line (AKR-MCA) with N,N-dimethylformamide (DMF) results in a reversion to the nontransformed AKR-2B cell line phenotype. AKR-MCA cells grown in the presence of 1% DMF showed a 2-fold increase in the sites for epidermal growth factor (EGF) binding. However, most of these sites were occupied by an endogenous ligand. The EGF receptor was unoccupied in untreated AKR-MCA cells. The increased receptor occupation was paralleled by an increase in the mitogenic response to EGF. Treatment of these cells with 1% DMF resulted in a 6-fold stimulation of mitogenesis by EGF. The ability to respond to nutrient replenishment (a property of growth-arrested AKR-MCA cells) was lost within 24 h of DMF treatment. Upon removal of DMF from the cells, both the mitogenic response to EGF and the occupation of the EGF receptor by endogenous ligands were lost. Treatment of the AKR-2B cell line with DMF had little effect on its growth properties. Therefore, DMF altered the growth control response and growth factor binding of AKR-MCA cells in a reversible, noncytotoxic manner.

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Supported by Grant PDT-109 from the American Cancer Society, Grants CA34432 and CA38100 from the NIH, and Grant RR-05425 from the USPHS.

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