In the metastatic process, various cell-
cell adhesion molecules seem to play an important role.
E-cadherin, a transmembrane
protein with an extracellular and an intracellular domain, is one of the key players involved in cell-cell adhesion. The function of
E-cadherin in preventing
metastasis in tumour development is believed to be dependent on intracellular
catenins. In a previous study, the expression of
E-cadherin was examined in a series of human
breast carcinomas. In that study, down-regulation of
E-cadherin failed to correlate with lymph node and/or distant
metastasis. In the present study, the expression of alpha-, beta-, and gamma-
catenins has been examined in a subset of the same tumours in order to evaluate their possible role in
breast cancer metastasis. Tumour tissues from 90 primary
breast carcinomas were immunostained for alpha-, beta-, and gamma-
catenins. Reduced or absent immunoreactivity in the tumour tissue was seen in 63 (70.0 per cent) for
alpha-catenin, in 50 (55.6 per cent) for
beta-catenin, and in 50 (55.6 per cent) for
gamma-catenin. Reduced expression of each of the
catenins alone failed to correlate to
metastasis. However, when all of the four
proteins (
E-cadherin,
alpha-catenin,
beta-catenin, and
gamma-catenin) were analysed as one group, a significant association was seen between reduction in immunoreactivity of at least one of these four
proteins and the presence of
metastases. These results indicate that if one of these
proteins is down-regulated, the function of the others in suppressing
metastasis is altered. A significant association was seen between lobular invasive tumours and
beta-catenin expression.