Defective E-cadherin function in urological cancers: clinical implications and molecular mechanisms.
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. E-cadherin is an epithelial cell-cell adhesion molecule and impaired function presumably 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, posttranslational modification or changes in the interaction of E-cadherin with cytoskeleton anchoring proteins--the catenins. A major mechanism leading to decreased E-cadherin expression in tumors 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 normal expression.
Giroldi
L A
LA
Urological Research Laboratory, University Hospital Nijmegen, The Netherlands.
Bringuier
P P
PP
Schalken
J A
JA
D000818:Animals; D015820:Cadherins / Q000032:analysis / Q000502:physiology*; D002450:Cell Communication / Q000502:physiology; D005109:Extracellular Matrix / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D011379:Prognosis; D011471:Prostatic Neoplasms / Q000737:chemistry / Q000473:pathology* / Q000503:physiopathology; D001749:Urinary Bladder Neoplasms / Q000737:chemistry / Q000473:pathology* / Q000503:physiopathology
D015820:Cadherins