Changes in Receptor Occupancy and Growth Factor Responsiveness Induced by Treatment of a Transformed Mouse Embryo Cell Line with N,N-Dimethylformamide

Alan E. Levine, L. J. McRae, Michael G Brattain

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Abstract

Treatment of the transformed mouse embryo fibroblast cell line (AKR-MCA) with N,A/-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 2fold 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.

Original languageEnglish (US)
Pages (from-to)6401-6405
Number of pages5
JournalCancer Research
Volume45
StatePublished - Dec 1 1985

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Dimethylformamide
Growth Factor Receptors
Embryonic Structures
Cell Line
Epidermal Growth Factor
Epidermal Growth Factor Receptor
Growth
Ligands
Occupations
Intercellular Signaling Peptides and Proteins
Fibroblasts
Phenotype
Food

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Changes in Receptor Occupancy and Growth Factor Responsiveness Induced by Treatment of a Transformed Mouse Embryo Cell Line with N,N-Dimethylformamide. / Levine, Alan E.; McRae, L. J.; Brattain, Michael G.

In: Cancer Research, Vol. 45, 01.12.1985, p. 6401-6405.

Research output: Contribution to journalArticle

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abstract = "Treatment of the transformed mouse embryo fibroblast cell line (AKR-MCA) with N,A/-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 2fold 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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AB - Treatment of the transformed mouse embryo fibroblast cell line (AKR-MCA) with N,A/-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 2fold 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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