Molecular analysis of E-cadherin and cadherin-11 in Wilms' tumours

J Pathol. 2000 Jun;191(2):162-9. doi: 10.1002/(SICI)1096-9896(200006)191:2<162::AID-PATH604>3.0.CO;2-8.


Different studies of Wilms' tumours have demonstrated a loss of heterozygosity (LOH) of chromosome 16q ranging from 17 to 25%. In order to search for a potential tumour suppressor gene on 16q, we chose the calcium-dependent cell adhesion molecules E-cadherin and cadherin-11 as candidate genes, which are both located on the long arm of chromosome 16. E-cadherin is known to be expressed in epithelial structures, whereas cadherin-11 is supposed to be expressed in mesenchymal structures and developing epithelium, including renal tubules. For the present study, fresh frozen tissue from 30 Wilms' tumours and corresponding non-tumour tissues were analysed. Single nucleotide polymorphisms of the E-cadherin and cadherin-11 genes were chosen and analysed for allelic inactivation by polymerase chain reaction (PCR) amplification and sequence analysis. Loss of expression of one E-cadherin allele was seen in 10% (2/20) of the informative cases. Two out of 11 informative cases (18%) showed loss of expression of one cadherin-11 allele. No length alterations of either the E-cadherin or the cadherin-11 messenger RNAs were identified using reverse transcription PCR and agarose gel electrophoresis in tumour tissue. Sequencing of the entire E-cadherin coding region in seven cases showed the wild-type sequence. These data imply that E-cadherin and cadherin-11 are not likely to play typical tumour suppressor roles in Wilms' tumour. Interestingly, the E-cadherin immunohistochemistry showed a deviation from the normal reaction pattern in 50% of the cases, with 27% (8/30) showing an apical or cytoplasmic reaction and 23% (7/30) being completely negative. Northern blot analysis revealed that the overall expression of cadherin-11 is much stronger than that of E-cadherin. In several cases, the expression levels of the two genes were inversely correlated, suggesting the existence of a regulatory mechanism. Analysis of differential expression of the various cadherins and their subsequent signal transduction pathways might contribute to a better understanding of the complexity of Wilms' tumour formation.

MeSH terms

  • Adolescent
  • Adult
  • Blotting, Northern
  • Cadherins / genetics*
  • Case-Control Studies
  • Child
  • Child, Preschool
  • Chromosomes, Human, Pair 16 / genetics*
  • Electrophoresis, Agar Gel
  • Female
  • Gene Expression Profiling
  • Gene Silencing
  • Humans
  • Infant
  • Infant, Newborn
  • Kidney Neoplasms / genetics*
  • Loss of Heterozygosity
  • Male
  • Polymorphism, Genetic
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sequence Analysis, DNA
  • Wilms Tumor / genetics*


  • Cadherins
  • osteoblast cadherin