P53 TUMOR-SUPPRESSOR GENE AND CYCLIC ADENOSINE-MONOPHOSPHATE IN BREAST AND ESOPHAGEAL CANCER ARE REGULATED THROUGH HIGH-CONCENTRATION OF EPIDERMAL GROWTH-FACTOR

1993 ◽  
Author(s):  
Y MURAYAMA
Keyword(s):  
Esophageal Cancer ◽  
Growth Factor ◽  
Tumor Suppressor ◽  
Epidermal Growth Factor ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Suppressor Gene ◽  
High Concentration ◽  
P53 Tumor Suppressor Gene ◽  
Epidermal Growth

Epidermal growth factor stimulates the prolactin synthesis and secretion in rat pituitary cells in culture (GH4C1 cells) by increasing the intracellular concentration of free calcium

1993 ◽  
Vol 128 (4) ◽  
pp. 361-366 ◽  
Author(s):  
Marie Aanestad ◽  
J Sigurd Røtnes ◽  
Peter A Torjesen ◽  
Egil Haug ◽  
Olav Sand ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Intracellular Concentration ◽  
Free Calcium ◽  
Pituitary Cells ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Epidermal Growth

Epidermal growth factor (EGF) stimulated the prolactin (PRL) synthesis and release from the GH4C1 cells in a dose-dependent manner. The ED50 was between 10−11 and 10−10 mol/l. The maximal effect was obtained at 10−9 mol/l EGF for the release, and 10−8 mol/l EGF for the synthesis. EGF stimulated the release of PRL from cell perfusion columns after a lag period of about 30 s. The maximal secretion of PRL occurred about 60 s after the start of stimulation. The PRL secretion declined to basal levels within 2 min. The EGF-stimulated PRL release was additive to the secretion evoked by thyrotropin-releasing hormone (TRH) and vasoactive intestinal peptide (VIP). An instantaneous increase in the intracellular concentration of free calcium, [Ca2+]i, of the GH4C1 cells was observed after the administration of EGF. EGF modified neither the basal nor the TRH-stimulated inositoltrisphosphate production in the GH4C1 cells, and EGF did not show any effect on the cyclic adenosine monophosphate production of these cells.

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