Altered distribution of β-catenin has been found in many human malignancies including gastric cancer, but its reason(s) and biological implications have not yet been fully clarified. By the methods of frozen tissue array-based immunohistochemistry, RT-PCR and PCR-SSCP followed by DNA sequencing, the patterns of β-catenin distribution in the subtypes of gastric cancers and their premalignant and non-cancerous counterparts were examined and the potential correlation of β-catenin alteration with invasion was elucidated. Membranous β-catenin was detected constantly in non-cancerous mucosa but became reduced or absent in cancer tissues. The cytoplasmic and nuclear accumulation of β-catenin could be observed in premalignant (atrophic gastritis and intestinal metaplasia) and cancer tissues, particularly in those infiltrated into deep muscular region. β-catenin mutation was not detected in all of tissue samples with and without translocalized β-catenin. These results indicate that β-catenin translocalization is a common phenomenon in gastric cancers as well as their related lesions. The loss of membranous and the gain of cytoplasmic and nuclear β-catenin in gastric cancers checked in this study are not due to the mutational event. β-catenin molecules translocalized in the nuclei are closely correlated with tumor invasion.

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