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Helicobacter pylori infection promotes methylation and silencing of trefoil factor 2, leading to gastric tumor development in mice and humans.

Anthony J Peterson1, Trevelyan R Menheniott, Louise O'Connor

  • 1Murdoch Children's Research Institute, Royal Children's Hospital, Flemington Road, Parkville, Victoria.

Gastroenterology
|August 31, 2010

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View abstract on PubMed

Summary

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  • Biomedical And Clinical Sciences
  • Oncology And Carcinogenesis
  • Predictive And Prognostic Markers
  • Helicobacter Pylori Infection Promotes Methylation And Silencing Of Trefoil Factor 2, Leading To Gastric Tumor Development In Mice And Humans.
    • This summary is machine-generated.

    Trefoil factor 2 (TFF2) is silenced by promoter methylation during H. pylori infection, which accelerates gastric preneoplasia and tumor development. Restoring TFF2 expression inhibits tumor growth.

    Area of Science:

    • Gastroenterology
    • Molecular Biology
    • Oncology

    Background:

    • Trefoil factors (TFFs) are crucial for gastric mucosal repair and tumor suppression.
    • TFF2 expression loss is common in gastric neoplasms, but the silencing mechanism and its role in tumorigenesis are unclear.

    Purpose of the Study:

    • To investigate the epigenetic silencing of TFF2 in gastric conditions.
    • To determine the impact of TFF2 deficiency on gastric tumor development.

    Main Methods:

    • Analyzed TFF2 promoter methylation in human gastric biopsies from various disease states.
    • Manipulated TFF2 methylation and expression in gastric cancer cell lines.
    • Studied Tff2 deficiency effects in a mouse model of gastric cancer and with experimental H. pylori infection.

    Main Results:

    • TFF2 promoter methylation increases with H. pylori infection and gastric tumor progression, inversely correlating with TFF2 mRNA levels.
    • Demethylation restored TFF2 expression in cell lines, confirming methylation-dependent silencing.
    • Tff2 deficiency in mice accelerated preneoplasia, increased mucosal cell proliferation, and altered cytokine profiles.

    Conclusions:

    • TFF2 acts as a tumor suppressor in the stomach.
    • H. pylori-induced promoter methylation of TFF2 subverts its tumor-suppressive role, promoting preneoplastic progression.

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