Premium
Inhibition of epidermal growth factor receptor stimulates prolactin expression in primary culture of the mouse pituitary gland
Author(s) -
Nogami Haruo,
Koshida Ryusuke,
Omori Hiroyuki,
Shibata Masahiro,
Harigaya Toshio,
Takei Yosuke
Publication year - 2019
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/jne.12764
Subject(s) - medicine , endocrinology , prolactin , epidermal growth factor , erlotinib , pituitary gland , biology , receptor , cell culture , northern blot , prolactin cell , gene expression , epidermal growth factor receptor , hormone , gene , biochemistry , genetics
The roles of epidermal growth factor ( EGF ) in the regulation of prolactin ( PRL ) gene expression in the normal pituitary gland remain poorly understood. In the present study, the effects of EGF and an inhibitor of the EGF receptor, erlotinib, on PRL gene expression were examined both in the pituitary tumour cell line GH 3 and in a primary culture of the mouse pituitary gland under similar experimental conditions. The results showed that EGF stimulated PRL expression in GH 3 cells, but not in normal cells. Erlotinib was found to counteract EGF in GH 3 cells inhibiting the PRL expression enhanced by EGF . By contrast, erlotinib induced an elevation in the PRL mRNA levels in the primary culture of the adult pituitary gland and the initiation of PRL production in the culture of the foetal pituitary gland in which PRL production had not yet occurred. Western blot analyses showed that EGF induced and erlotinib inhibited the activation of extracellular regulated protein kinase equally in GH 3 and normal cells. These results suggest that the consequences of EGF receptor activation in normal PRL cells contradict those in adenomatous PRL cells.