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β-Catenin mediates the interaction of E-cadherin with α-catenin and the actin cytoskeleton. Recent evidence indicates that when the tumor suppressor gene APC is inactivated, β-catenin can translocate to the nucleus, where it acts as a transcriptional regulator. Because APC is inactivated in most colorectal cancers, β-catenin nuclear localization would be expected in these tumors. In a study of adhesion molecule expression in frozen colorectal cancer tissues, we were surprised by failure to detect nuclear β-catenin. Here we compared the reactivity of an anti-β-catenin monoclonal antibody with 11 colorectal cancers using immunohistochemistry on sections of frozen or paraffin-embedded samples. β-Catenin was never detected in the nuclei of normal or tumor cells in frozen tissue sections. By contrast, in 8/11 cases it was detected in the nuclei of tumor cells but not of normal cells in paraffin-embedded tissue sections. These results were confirmed with an independent rabbit polyclonal anti-β-catenin serum. We also examined β-catenin distribution in SW480 colon cancer cells, in which its nuclear accumulation has been reported. As in tissues, nuclear β-catenin was detected in paraffin-embedded but not in frozen samples. These findings are relevant because of the increasing interest in the study of β-catenin in tumors, based on its dual role in cell adhesion and transcriptional regulation. (J Histochem Cytochem 47:1089–1094, 1999)

Nuclear β-catenin in Colorectal Tumors: To Freeze or Not To Freeze?