Helicobacter pylori can induce heparin-binding epidermal growth factor expression via gastrin and its receptor

Jacqueline H Dickson, Anna Grabowska, Mohamad El-Zaatari, John Atherton, Susan A Watson

Research output: Contribution to journalArticlepeer-review


Both gastrin and Helicobacter pylori have been shown capable of up-regulating gene expression and protein shedding of heparin-binding epidermal growth factor (HB-EGF). Furthermore, the bacteria have previously been shown to induce serum hypergastrinemia in infected individuals. The aim of this work was to assess the extent to which the ability of H. pylori to up-regulate expression of HB-EGF can be attributed to its effect on gastrin. Gastric cells, transfected with either gastrin small interfering RNA or antisense plasmid or the gastrin/cholecystokinin-2 receptor (CCK-2R), were cultured for 24 hours with H. pylori(+/-), a CCK-2R antagonist. Gene expression levels were measured using reverse transcription-PCR, whereas protein changes were measured using ELISA, Western blotting, and immunofluorescence. H. pylori induced significantly higher levels of HB-EGF gene expression and ectodomain shedding in the CCK-2R-transfected cells than the vector control (P
Original languageEnglish
Pages (from-to)7524-31
Number of pages8
JournalCancer Research
Issue number15
Publication statusPublished - 1 Aug 2006


  • Adenocarcinoma
  • Animals
  • Cell Line, Tumor
  • DNA, Antisense
  • Disease Models, Animal
  • Enterochromaffin Cells
  • Epidermal Growth Factor
  • Gastrins
  • Helicobacter Infections
  • Helicobacter pylori
  • Humans
  • Intercellular Signaling Peptides and Proteins
  • Mice
  • Plasmids
  • RNA, Small Interfering
  • Receptor, Cholecystokinin B
  • Reverse Transcriptase Polymerase Chain Reaction
  • Stomach Neoplasms
  • Transfection
  • Up-Regulation


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