Involvement of adenomatous polyposis coli (APC)/beta-catenin signalling in human breast cancer

M Jönsson, A Borg, M Nilbert, T Andersson

Research output: Contribution to journalArticlepeer-review

Abstract

We studied the relevance of adenomatous polyposis coli (APC)/beta-catenin signalling in the development of breast cancer by analysing the expression of beta-catenin in 54 primary breast tumours (34 ductal and 20 lobular). We showed that 13% of the tumours exhibited upregulated levels of beta-catenin in the cytosol suggesting that defects in APC/beta-catenin signalling components had lowered the rate of beta-catenin degradation. No mutations were observed in the amino-terminal region of beta-catenin, which comprises conserved serine residues important for phosphorylation-dependent degradation of the protein, but the APC protein was altered in 6% of the tumours. Tyrosine phosphorylation of beta-catenin was detected in only one tumour and could, therefore, not have been responsible for the observed increased levels of this protein. Although 9% of the tumours displayed upregulation of c-MYC protein, there was no correlation with beta-catenin overexpression, suggesting that increased beta-catenin expression is not the major cause of c-myc gene activation in breast cancer. It is imperative that elements that selectively drive the oncogenic activity of beta-catenin in breast cancer be identified.

Original languageEnglish
Pages (from-to)242-8
Number of pages7
JournalEuropean Journal of Cancer
Volume36
Issue number2
Publication statusPublished - 2000 Jan

Subject classification (UKÄ)

  • Cancer and Oncology

Free keywords

  • Adenomatous Polyposis Coli Protein
  • Adult
  • Blotting, Western
  • Breast Neoplasms/genetics
  • Carcinoma, Ductal, Breast/genetics
  • Carcinoma, Lobular/genetics
  • Cell Communication
  • Cytoskeletal Proteins/metabolism
  • Female
  • Humans
  • Mutation/genetics
  • Neoplasm Proteins/metabolism
  • Sweden
  • Trans-Activators
  • beta Catenin

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