Anticancer research · 2005
E-cadherin and beta-catenin expression in normal, inflamed and cancerous gallbladder tissue.
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Puhalla Harald, Herberger Beate, Soleiman Afschin, Filipits Martin, Laengle Fritz, Gruenberger Thomas, Wrba Fritz
Аннотация
BACKGROUND: Changes of the E-cadherin/beta-catenin complex during cell-cell interactions result in the loss of cell adhesion and may account for the ability of cancer cells to metastasize. Gallbladder carcinoma (GBC) can develop during chronic inflammation from normal tissue. The aim of this study was to investigate the expression of E-cadherin and beta-catenin in normal gallbladder mucosa, inflamed gallbladder tissue and GBC.
MATERIALS AND METHODS: Tissue from 10 GBC, 10 chronic cholecystitis and 10 healthy gallbladders were used to evaluate the expression of E-cadherin and beta-catenin by immunohistochemistry.
RESULTS: The beta-catenin membranous expression decreased between cholecystitis and malignant tissue, as well as between normal epithelium and carcinoma. The E-cadherin membranous expression was reduced in normal gallbladder epithelia compared to carcinoma and also from inflammation to GBC. The cytoplasmatic beta-catenin expression did not show any significant difference. Cytoplasmatic E-cadherin was significantly different from normal gallbladders to carcinomas and between normal tissue and inflammation. No significant difference of the nuclear P-catenin expression could be observed. E-cadherin was not detected intra-nuclear in any tissue.
CONCLUSION: Significant differences of E-cadherin and beta-catenin were detected between normal, inflamed and cancerous tissues. These changes of the protein expressions and the associated loss of adhesive mechanisms might lead to a cancerous pathway in GBC.
MATERIALS AND METHODS: Tissue from 10 GBC, 10 chronic cholecystitis and 10 healthy gallbladders were used to evaluate the expression of E-cadherin and beta-catenin by immunohistochemistry.
RESULTS: The beta-catenin membranous expression decreased between cholecystitis and malignant tissue, as well as between normal epithelium and carcinoma. The E-cadherin membranous expression was reduced in normal gallbladder epithelia compared to carcinoma and also from inflammation to GBC. The cytoplasmatic beta-catenin expression did not show any significant difference. Cytoplasmatic E-cadherin was significantly different from normal gallbladders to carcinomas and between normal tissue and inflammation. No significant difference of the nuclear P-catenin expression could be observed. E-cadherin was not detected intra-nuclear in any tissue.
CONCLUSION: Significant differences of E-cadherin and beta-catenin were detected between normal, inflamed and cancerous tissues. These changes of the protein expressions and the associated loss of adhesive mechanisms might lead to a cancerous pathway in GBC.