Truncated APC is required for cell proliferation and DNA replication

Int J Cancer. 2006 Jul 1;119(1):74-9. doi: 10.1002/ijc.21826.


The tumour suppressor APC is truncated in most colon cancers, which leads to the stabilization of beta-catenin and to the constitutive activation of Wnt signalling. However, it is not clear why colon cancer cells retain the truncated APC fragment. Here, we show that a decrease of APC levels achieved by RNA interference impairs cell proliferation and DNA replication, not only in 293 cells that express a wild-type protein, but also in SW480 colon cancer cells that express exclusively a truncated APC fragment. This correlates with a reduction of the levels of cyclin A, cyclin A-dependent kinase activity, p27(kip1) and the catalytic subunit of DNA polymerase delta. Thus, our data suggest that colon cancer cells retain a truncated APC fragment because it is essential for cell proliferation.

MeSH terms

  • Cell Cycle
  • Cell Proliferation*
  • Colonic Neoplasms / genetics*
  • Colonic Neoplasms / metabolism*
  • Cyclin A / metabolism
  • Cyclin-Dependent Kinase Inhibitor p27 / metabolism
  • DNA Polymerase III / metabolism
  • DNA Replication*
  • Gene Expression Regulation, Neoplastic
  • Genes, APC*
  • Humans
  • Protein Kinases / metabolism
  • RNA Interference
  • Signal Transduction
  • Tumor Cells, Cultured
  • Wnt Proteins / genetics
  • Wnt Proteins / metabolism
  • beta Catenin / genetics
  • beta Catenin / metabolism


  • Cyclin A
  • Wnt Proteins
  • beta Catenin
  • Cyclin-Dependent Kinase Inhibitor p27
  • Protein Kinases
  • histone H1 kinase
  • DNA Polymerase III