Aberrant signalling activities of beta -catenin, originally identified as a
component of cell-adhesion complexes, are now considered to be an importan
t factor in colorectal carcinogenesis. However, recently it was shown that
also gamma- as well as p120 catenins have a dual role either in cell adhesi
on or in affecting some gene activation. Therefore, the levels and interact
ions of these three catenins in human colorectal carcinoma cell lines were
analysed. A great heterogeneity in the expression of all catenins tested wa
s found in colorectal carcinoma cell lines HT29 and LS174T. Detailed analys
is of beta -catenin interactions was done. GST-APC fragment-fused proteins
were used to absorb beta -catenin and its complexes from cell lysates. Simi
larly, the E-cadherin binding capacity of the residual pool of beta -cateni
n was analysed using the GST-ECT construct. It was found that the level of
beta -catenin does not necessarily depend either on the APC or beta -cateni
n gene mutations and that co-precipitation of beta-, gamma-, and p120 caten
ins is not limited to cells that express E-cadherin.