Classical cadherins in urological cancers.

Decreased E-cadherin expression assessed by immunohistochemistry correlates with poor survival of bladder and prostate cancer patients. The clinical usefulness of this parameter should therefore be evaluated in a large scale prospective study. In proximal kidney tubule and in its derived tumours cadherin-6 seems to take over E-cadherin function. Impaired E-cadherin function leads to increased invasive capacity of the cells. It has been shown that defective function can result from several mechanisms: mutation of the gene, alteration of transcription, post translational modifications or changes in the interaction of E-cadherin with cytoskeleton anchoring proteins: the catenins. A major mechanism leading to decreased E-cadherin expression in tumours lies in decreased transcription of the gene. Hence, a better understanding of the regulation of E-cadherin transcription might open avenues for therapy by restoring a normal expression.