Work

Autocrine stimulation of AR4-2J rat pancreatic tumor cell growth by glycine-extended gastrin

Year: 1996

Type: article

Abstract: Glycine-extended gastrin (gastrin-Gly) stimulates proliferation of AR4-2J pancreatic tumor cell line through a specific receptor, different from the gastrin-cholecystokinin B receptor. Our purpose was to determine whether AR4-2J cells produced gastrin-Gly and then whether the peptide was involved in an autocrine loop. First, proliferation of AR4-2J cells in serum-free medium was inhibited by a gastrin anti-sense oligodeoxynucleotide phosphorothioate and by antibodies specific for gastrin-Gly. In contrast, antibodies specific for alpha-amidated gastrin were without effect. By using RT-PCR, we have shown that AR4-2J cells expressed gastrin mRNA. The presence of gastrin-Gly, but not alpha-amidated gastrin, in serum-free media was detected by radioimmunoanalysis. Gel chromatography revealed that the predominant molecular forms secreted were glycine-extended gastrin-34 and gastrin- 17. Furthermore, epidermal growth factor (EGF), a stimulator of gastrin gene transcription, modulates gastrin-Gly secretion by AR4-2J. These data together suggest that gastrin-Gly is an autocrine growth factor for AR4-2J cells and that it participates with EGF in the regulation of AR4-2J-cell proliferation.

Source: International Journal of Cancer

DOI: 10.1002/(sici)1097-0215(19960529)66:5<653::aid-ijc12>3.0.co;2-5

Authors: Fabrice Nègre, Pierrette Fagot-Revurat, Michèle Bouisson, Jens F. Rehfeld, Nicole Vaysse, Lucien Pradayrol

Institutions: Inserm, Centre Hospitalier Universitaire de Toulouse, Hôpital Rangueil, Rigshospitalet

Language: English

Topic: Neuropeptides and Animal Physiology

Subfield: Cellular and Molecular Neuroscience

Field: Neuroscience

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: bronze

Funder: Association pour la Recherche sur le Cancer