Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

GIP (EC50 = 8 X 10(-9) M, 5-fold stimulation), pancreatic glucagon (EC50 = 10(-8)M, 13-fold) and porcine or chicken VIP (EC50 = 2.5 X 10(-9) M, 10-fold) are shown to activate the cAMP generating system in HGT -1 cells. Combinations of GIP, pancreatic glucagon and VIP indicate the occurrence of 3 separate sets of recognitions sites for these 3 peptides. Accordingly, chronic treatment of cultured HGT -1 cells by VIP (10(-8) M) during 6 days resulted in homologous desensitization of VIP receptor activity. Other peptides structurally related to the secretin-glucagon family, to neurotensin, or to gastrin are either ineffective or very weak agonist (hpGRF). GIP or pancreatic glucagon are inactive on the human colonic cell line HT-29, indicating the gastric specificity of the effect of GIP and glucagon in transformed epithelial cells originating from the human gastrointestinal tract. This implies that GIP and (pancreatic-entero) glucagon peptides may regulate gastric secretions directly, under similar mechanisms that those we evidenced in the rat.
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PMID:Gastric inhibitory peptide (GIP), pancreatic glucagon and vasoactive intestinal peptide (VIP) are cAMP-inducing hormones in the human gastric cancer cell line HGT-1. Homologous desensitization of VIP receptor activity. 632 77

The growth of the human gastric cancer cell line HGT-1 is regulated by a gastrin-like peptide through an autocrine process. In order to analyse the mechanism of action of this peptide, a study at different steps of the cell cycle was considered; so, a blocking of this cell line by thymidine or hydroxy-urea was studied by cytofluorimetry. In normal growth conditions in 10% FCS medium, 57% of the cells were in G0/G1 phase and 31% in S phase. A treatment with 2 mM hydroxy-urea followed by 4 hours in 10% FCS medium led to 85% of the cells in S phase. By successive treatments with thymidine and hydroxy-urea followed by 1 hour in 10% FCS medium, 2 peaks of S phase corresponding to 86% of the cells were observed; after 24 hours, cells were distributed as found for the unconfluent cell line, whatever the treatment. On the other hand, the thymidine kinase activity of unconfluent cells which was relatively elevated as compared to other cell lines (278 mU/mg protein), was increased by synchronisation with hydroxyurea followed by 1 hour in 10% SVF medium (338 mU/mg protein); after 8 hours in 10% FCS medium, this activity decreased at the value observed for cells treated with thymidine followed by 1 hour in 10% FCS medium (214 mU/mg protein). In conclusion, a synchronisation either by thymidine or by hydroxy-urea, led to a blocking of the HGT-1 cell line at different steps of the cell cycle, leading to a better knowledge of its autocrine growth regulation.
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PMID:[Study of S phase synchronization of the human gastric cancer line HGT-1]. 806 18

Gastrin has been shown to promote the growth of some colonic tumor cell lines. To evaluate the involvement of this hormone in the proliferation of gastric tumors, we studied the effects of gastrin/CCK-receptor antagonists (L365,260 and L364,718), proglumide and C terminal-specific gastrin antibodies on the human gastric adenocarcinoma cell line HGT-1. L365,260, but not L364,718, dose-dependently inhibited cell proliferation (72% after 4 days at 10 nM) and [3H]thymidine incorporation (68% after 2 days at 10 nM) in serum-free medium. No cytotoxic effects of proglumide or L365,260 on this cell line were detected. Proglumide inhibited cell proliferation in serum-free medium (40% and 66.5% after 2 and 4 days of treatment; IC50 = 1.4 mM) and in 5% fetal calf serum (FCS)-supplemented medium (30% and 22% after 2 and 4 days of treatment; IC50 = 3.25 mM). [3H]Thymidine incorporation was also inhibited by proglumide in serum-free medium (IC50 = 2.3 mM) and 5% FCS-supplemented medium (IC50 = 3.35 mM). Gastrin did not induce cell proliferation or increase [3H]thymidine incorporation and no high-affinity gastrin binding sites were observed. However, C terminal-specific gastrin antibodies, even at low concentration, caused a dramatic decrease in both cell number (IC50 = 1:4000 antiserum dilution) and [3H]thymidine incorporation (IC50 = 1:400 antiserum dilution) in the HGT-1 cell line. In addition, immunofluorescence analysis revealed that these antibodies specifically bind HGT-1 cells and radioimmunoassay analysis confirms the presence of gastrin/CCK-like peptide in cell extracts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for autocrine growth stimulation by a gastrin/CCK-like peptide of the gastric cancer HGT-1 cell line. 831 31

We have previously shown that angiotensin I-converting enzyme (ACE) was expressed by epithelial cells of the rabbit gastric mucosa. In a search to obtain a cell model to study the regulation of ACE expression of gastric origin and its relationship with gastrin-cholecystokinin peptides, which have been proposed as ACE substrates, we investigated whether the HGT-1 human gastric cell line, which expresses gastrin, could also express ACE, using enzymatic and immunodetection methods as well as Northern-blot analysis and polymerase chain reaction. Results show that HGT-1 cells expressed a protein with a molecular weight of 130-140 kDa whose enzymatic and immunological properties were identical to those of ACE. More than 80% of ACE activity was found to be ectoenzymatic. However, immunocytochemical localization has mainly shown an intracellular localization, suggesting that most of intracytoplasmic ACE was not enzymatically active. In addition, Northern-blot analysis and polymerase chain reaction showed that the mRNA encoding that protein displayed a size and a sequence identical to those of somatic ACE. It therefore appears that the HGT-1 cell line could be a useful model to study both the regulation of gastric ACE and its interactions with gastrin-cholecystokinin peptides.
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PMID:Expression of angiotensin I-converting enzyme in the human gastric HGT-1 cell line. 857 43