Transfection of the Helicobacter pylori CagA gene alters MUC5AC expression in human gastric cancer cells.

Helicobacter pylori, the primary causative agent of stomach cancer, is known to affect gastric mucin expression. However, the underlying molecular mechanisms mediating this H. pylori-dependent effect remain unknown. In the present study, the effect of exogenous expression of the H. pylori virulence factor, CagA, on mucin 5AC oligomeric muscus/gel-forming (MUC5AC) expression was investigated using an in vitro model of the gastric mucosa. AGS cells were either untreated or transfected by a vector control (pCDNA3.1) or heterologous DNA, which induced CagA overexpression (pCDNA3.1-CagA). The expression and functionality of MUC5AC was analyzed using the reverse transcription-quantitative polymerase chain reaction and immunofluorescence assays. The expression of H. pylori-CagA in AGS cells was able to significantly upregulate MUC5AC expression compared to the vector control. In addition, immunofluorescence assays were able to validate increased MUC5AC expression following exogenous expression of H. pylori-CagA. The results of the present study revealed that the H. pylori-derived virulence factor CagA was able to increase the expression of MUC5AC. As this mucin constitutes an important ecological niche for H. pylori, this response may be involved in H. pylori colonization of the stomach.