Infection with Helicobacter pylori is a risk factor for the development of gastric cancer.
Dr Tsutomu Chiba and colleagues from Japan assessed infection of gastric epithelial cells with 'cag' pathogenicity island-positive H pylori.
The team showed that this infection induced aberrant expression of activation-induced cytidine deaminase.
|H pylori-mediated enzyme upregulation alters TP53 tumor suppressor genes|
Activation-induced cytidine deaminase is a member of the cytidine-deaminase family that acts as a DNA- and RNA-editing enzyme.
The enzyme edits DNA and RNA via the IKB kinase-dependent nuclear factor-KB activation pathway.
The researchers observed the effect of H pylori-mediated upregulation of activation-induced cytidine deaminase.
The team found that it leads to accumulation of nucleotide alterations in the TP53 tumor suppressor gene in gastric cells in vitro.
Dr Chiba's team concludes, “Our findings provide evidence that aberrant activation-induced cytidine deaminase expression might be a mechanism of mutation accumulation in the gastric mucosa during H pylori-associated gastric carcinogenesis.”
”The aberrant enzyme expression is caused by H pylori infection.”