ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2008
Gastrin increases mcl-1 expression in type I gastric carcinoid tumors and a gastric epithelial cell line that expresses the CCK-2 receptor.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Gastrin: From Physiology to Gastrointestinal Malignancies.Function (Oxford, England) · 2022Review
- Gastrin, Cholecystokinin, Signaling, and Biological Activities in Cellular Processes.Frontiers in endocrinology · 2020Review
- Hsa-miR-202-3p, up-regulated in type 1 gastric neuroendocrine neoplasms, may targetWorld journal of gastroenterology · 2018Article
- A cumulative effect involving malfunction of the PTH1R and ATP4A genes explains a familial gastric neuroendocrine tumor with hypothyroidism and arthritis.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2017Article
- Insights into gastric neuroendocrine tumors burden.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2017Article
- Endoscopic diagnosis and management of type I neuroendocrine tumors.World journal of gastrointestinal endoscopy · 2015Review
- Clinical features and management of type I gastric carcinoids.Clinical journal of gastroenterology · 2014Review
- MiR-148a regulates the growth and apoptosis in pancreatic cancer by targeting CCKBR and Bcl-2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- The duration of gastrin treatment affects global gene expression and molecular responses involved in ER stress and anti-apoptosis.BMC genomics · 2013Article
- Neuroendocrine phenotype alteration and growth suppression through apoptosis by MK-2206, an allosteric inhibitor of AKT, in carcinoid cell lines in vitro.Anti-cancer drugs · 2013Article
- Current concepts on gastric carcinoid tumors.Gastroenterology research and practice · 2012Article
- Gastric carcinoids: between underestimation and overtreatment.World journal of gastroenterology · 2009Article
- Importance of gastrin in the pathogenesis and treatment of gastric tumors.World journal of gastroenterology · 2009Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Elevated serum concentrations of the hormone gastrin are associated with the development of gastric carcinoid tumors, but the mechanisms of tumor development are not fully understood. We hypothesized that the antiapoptotic effects of gastrin may be implicated and have therefore investigated the role of antiapoptotic members of the bcl-2 family of proteins. AGS-G(R) human gastric carcinoma cells stably transfected with the CCK-2 receptor were used to assess changes in the expression of bcl-2 family members following gastrin treatment and the function of mcl-1 during apoptosis was investigated by use of small-interfering RNA (siRNA). Treatment of AGS-G(R) cells with 10 nM gastrin for 6 h caused maximally increased mcl-1 protein abundance. Gastrin-induced mcl-1 expression was inhibited by the transcription inhibitor actinomycin D and by the protein synthesis inhibitor cycloheximide. Downstream signaling of mcl-1 expression occurred via the CCK-2 receptor, protein kinase C, and MAP kinase pathways, but not via PI 3-kinase. Transfection with mcl-1 siRNA significantly suppressed mcl-1 protein expression and abolished the antiapoptotic effects of gastrin on serum starvation-induced apoptosis. Mcl-1 protein expression was also specifically increased in the type I enterochromaffin-like cell carcinoid tumors of 10 patients with autoimmune atrophic gastritis and hypergastrinemia. Gastrin therefore signals via the CCK-2 receptor, protein kinase C, and MAP kinase to induce expression of antiapoptotic mcl-1 in AGS-G(R) cells, and mcl-1 expression is also increased in human hypergastrinemia-associated type I gastric carcinoid tumors. Gastrin-induced mcl-1 expression may therefore be an important mechanism contributing toward type I gastric carcinoid development.
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