ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2011
Human gastrin mRNA expression up-regulated by Helicobacter pylori CagA through MEK/ERK and JAK2-signaling pathways in gastric cancer cells.
Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 17 citations in OpenAlex.
- Gastrin: From Physiology to Gastrointestinal Malignancies.Function (Oxford, England) · 2022Review
- Gastrin and Gastric Cancer.Cellular and molecular gastroenterology and hepatology · 2017Review
- Enhanced expression of the M2 isoform of pyruvate kinase is involved in gastric cancer development by regulating cancer-specific metabolism.Cancer science · 2017Article
- Article
- Molecular classification of gastric adenocarcinoma: translating new insights from the cancer genome atlas research network.Current treatment options in oncology · 2015Review
- Helicobacter pylori infection, gastrin and cyclooxygenase-2 in gastric carcinogenesis.World journal of gastroenterology · 2014Review
- Expression of annexin-A1 and galectin-1 anti-inflammatory proteins and mRNA in chronic gastritis and gastric cancer.Mediators of inflammation · 2013Article
- Janus kinase 2 polymorphisms are associated with risk in patients with gastric cancer in a Chinese population.PloS one · 2013Article
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5 authors at 1 institution in 1 country.
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Abstract
backgroundHelicobacter pylori-cytotoxin-associated protein A (CagA) and gastrin are believed to play an important role in gastric carcinogenesis, but their interaction has been incompletely clear.
methodsWe constructed a eukaryotic expression vector pcDNA3.1/cagA and a luciferase reporter vector pGL/gastrin promoter, and then co-transfected them into gastric cancer AGS and SGC-7901 cells. The two kinds of gastric cancer cells were, respectively, infected with cagA-positive H. pylori NCTC11637, and then the gastrin promoter activity and gastrin mRNA level were detected with a Dual-Luciferase reporter assay system and quantitative reverse transcription polymerase chain reaction (RT-PCR), respectively. Next, after the MEK/ERK and JAK2-signaling pathway inhibitors, U0126 and AG490, were used to treat the two cell lines, or the ERK1 and JAK2 genes were knocked down by siRNAs (small interference RNAs) in the two cell lines, the gastrin promoter activity and gastrin mRNA level were observed again.
resultsThe results indicated that CagA could activate the gastrin promoter and up-regulate gastrin mRNA expression in AGS and SGC-7901 cells, but these effects could be inhibited by the inhibitors U0126 and AG490, and the CagA-induced gastrin mRNA expression was down-regulated in the cells whose ERK1 or JAK2 gene was knocked down.
conclusionGastrin promoter may be the transcriptional target of CagA, and CagA activates the gastrin promoter to up-regulate gastrin mRNA expression through the MEK/ERK and JAK1-signaling pathway in gastric cancer cells.
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