Control of Mammary Epithelial Cell DNA Synthesis by Epidermal Growth Factor, Cholera Toxin, and IGF-1: Specific Inhibitory Effect of Prolactin on EGF-Stimulated Cell Growth

1994 ◽  
Vol 210 (1) ◽  
pp. 102-106 ◽  
Author(s):  
Suzanne E. Fenton ◽  
Lewis G. Sheffield
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Epithelial Cell ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Cholera Toxin ◽  
Mammary Epithelial Cell ◽  
Inhibitory Effect ◽  
Mammary Epithelial ◽  
Epidermal Growth

scholarly journals Tyrosine Phosphorylation of Grb2: Role in Prolactin/Epidermal Growth Factor Cross Talk in Mammary Epithelial Cell Growth and Differentiation

2009 ◽  
Vol 29 (10) ◽  
pp. 2505-2520 ◽  
Author(s):  
Eric Haines ◽  
Parham Minoo ◽  
Zhenqian Feng ◽  
Nazila Resalatpanah ◽  
Xin-Min Nie ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Cell Growth ◽  
Epithelial Cell ◽  
Epidermal Growth Factor ◽  
Tyrosine Phosphorylation ◽  
Mammary Epithelial Cell ◽  
Mammary Epithelial ◽  
Cell Growth And Differentiation ◽  
Epidermal Growth

ABSTRACT Characterizing mechanisms regulating mammary cell growth and differentiation is vital, as they may contribute to breast carcinogenesis. Here, we examine a cross talk mechanism(s) downstream of prolactin (PRL), a primary differentiation hormone, and epidermal growth factor (EGF), an important proliferative factor, in mammary epithelial cell growth and differentiation. Our data indicate that EGF exerts inhibitory effects on PRL-induced cellular differentiation by interfering with Stat5a-mediated gene expression independent of the PRL-proximal signaling cascade. Additionally, our data show that PRL is a potent inhibitor of EGF-induced cell proliferation. We identify tyrosine phosphorylation of the growth factor receptor-bound protein 2 (Grb2) as a critical mechanism by which PRL antagonizes EGF-induced cell proliferation by attenuating the activation of the Ras/mitogen-activated protein kinase (MAPK) pathway. Together, our results define a novel negative cross-regulation between PRL and EGF involving the Jak2/Stat5a and Ras/MAPK pathways through tyrosine phosphorylation of Grb2.

The calcium signal for BALB/MK keratinocyte terminal differentiation counteracts epidermal growth factor (EGF) very early in the EGF-induced proliferative pathway

1988 ◽  
Vol 8 (2) ◽  
pp. 557-563
Author(s):  
P P Di Fiore ◽  
J Falco ◽  
I Borrello ◽  
B Weissman ◽  
S A Aaronson
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Fold Increase ◽  
Inhibitory Effect ◽  
Lymphoid Cells ◽  
Epidermal Keratinocytes ◽  
Calcium Signal ◽  
High Calcium ◽  
Epidermal Growth

BALB/MK mouse epidermal keratinocytes require epidermal growth factor (EGF) for proliferation and terminally differentiate in response to high calcium concentrations. We show that EGF is an extremely potent mitogen, causing BALB/MK cultures to enter the cell cycle in a synchronous manner associated with a greater than 100-fold increase in DNA synthesis. Analysis of the expression of proto-oncogenes which have been reported to be activated during the cascade of events following growth factor stimulation of fibroblasts or lymphoid cells revealed a very rapid but transient 100-fold increase in c-fos RNA but little or no effect on the other proto-oncogenes analyzed. Exposure of EGF-synchronized BALB/MK cells to high levels of calcium was associated with a striking decrease in the early burst of c-fos RNA as well as the subsequent peak of cell DNA synthesis. Since the inhibitory effect of high calcium on c-fos RNA expression was measurable within 30 min, our studies imply that the EGF proliferative and calcium differentiation signals must interact very early in the pathway of EGF-induced proliferation. Our results also establish that c-fos RNA modulation is an important early marker of cell proliferation in epithelial as well as mesenchymal cells.

scholarly journals Epidermal growth factor inhibits growth of A431 human epidermoid carcinoma in serum-free cell culture.

1982 ◽  
Vol 93 (1) ◽  
pp. 1-4 ◽  
Author(s):  
D W Barnes
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Epidermal Growth Factor ◽  
Culture Medium ◽  
Cell Types ◽  
Inhibitory Effect ◽  
Free Cell ◽  
Bovine Insulin ◽  
A431 Cell ◽  
Epidermal Growth

A medium consisting of a rich basal nutrient mixture supplemented with bovine insulin (10 micrograms/ml), human transferrin (10 micrograms/ml), human cold-insoluble globulin (5 micrograms/ml), and ethanolamine (0.5 mM) supported the growth of the A431 human epidermoid cell line in the absence of serum with a generation time equal to that of cells in serum-containing medium. Addition of epidermal growth factor (EGF) to this culture medium at concentration mitogenic for other cell types resulted in a marked inhibition of A431 cell growth. Inhibitory effects of EGF were observed at 1 ng/ml and near-maximal effects were observed at 10 ng/ml. The inhibitory effect of EGF could be reversed by the omission of EGF in subsequent medium changes and could be prevented by the addition of anti-EGF antibody to the culture medium. Inhibition of A431 cell growth by EGF also could be demonstrated in serum-containing medium.

scholarly journals The calcium signal for BALB/MK keratinocyte terminal differentiation counteracts epidermal growth factor (EGF) very early in the EGF-induced proliferative pathway.

1988 ◽  
Vol 8 (2) ◽  
pp. 557-563 ◽  
Author(s):  
P P Di Fiore ◽  
J Falco ◽  
I Borrello ◽  
B Weissman ◽  
S A Aaronson
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Fold Increase ◽  
Inhibitory Effect ◽  
Lymphoid Cells ◽  
Epidermal Keratinocytes ◽  
Calcium Signal ◽  
High Calcium ◽  
Epidermal Growth

BALB/MK mouse epidermal keratinocytes require epidermal growth factor (EGF) for proliferation and terminally differentiate in response to high calcium concentrations. We show that EGF is an extremely potent mitogen, causing BALB/MK cultures to enter the cell cycle in a synchronous manner associated with a greater than 100-fold increase in DNA synthesis. Analysis of the expression of proto-oncogenes which have been reported to be activated during the cascade of events following growth factor stimulation of fibroblasts or lymphoid cells revealed a very rapid but transient 100-fold increase in c-fos RNA but little or no effect on the other proto-oncogenes analyzed. Exposure of EGF-synchronized BALB/MK cells to high levels of calcium was associated with a striking decrease in the early burst of c-fos RNA as well as the subsequent peak of cell DNA synthesis. Since the inhibitory effect of high calcium on c-fos RNA expression was measurable within 30 min, our studies imply that the EGF proliferative and calcium differentiation signals must interact very early in the pathway of EGF-induced proliferation. Our results also establish that c-fos RNA modulation is an important early marker of cell proliferation in epithelial as well as mesenchymal cells.

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