The significance of beta-catenin, E-cadherin, and P-cadherin expressions in neoplastic progression of colorectal mucosa: an immunohistochemical study.

BACKGROUND AND STUDY AIMS

The purpose of the current study was to investigate the role of beta-catenin, E-cadherin and P-cadherin in colorectal carcinogenesis using tissue array method.

PATIENTS AND METHODS

Core tissue biopsies were taken from paraffin-embedded tissue blocks of 167 cases including 26 normal mucosae (NM), 99 colorectal polyps (10 hyperplastic polyps (HP), 8 traditional serrated (TSA), 17 tubular (TA), 37 tubulovillous (TVA), and 27 villous adenomas (VA)), 14 adenomas with intramucosal carcinoma (ACA), and 28 colorectal cancers (CCA). Immunohistochemistry was performed using antibodies to beta-catenin, E-cadherin, and P-cadherin. Distribution of positivity was assessed using percentage expression while an arbitrary grading scale was used for staining intensity.

RESULTS

beta-catenin expression was cytoplasmic, membranous, and nuclear. Both E-cadherin and P-cadherin expressions were confined to cytoplasmic-membranous compartments. Membranous expression of beta-catenin significantly decreased in CCA (p < 0.01). Nuclear beta-catenin expression significantly increased in close correlation with neoplastic sequence reaching its highest expression in ACA and CCA (p < 0.001). Polyps with intraepithelial neoplasia (IEN) showed significantly higher nuclear beta-catenin expression in parallel with increasing grades of IEN (p < 0.001). E-cadherin and P-cadherin expression increased in polyps, whereas a significant decrease in their expression was observed in CCA (p < 0.001) while E-cadherin expression significantly increased in CCA compared to NM (p < 0.001), no such difference was observed in P-cadherin expression.

CONCLUSIONS

Nuclear beta-catenin expression correlating with the grade of IEN in polyps and carcinomas supports its role in colorectal carcinogenesis. E-cadherin and P-cadherin expressions in adenomas suggest that these molecules might have role in adenoma formation though not necessarily be involved in neoplastic progression.