p27 is involved in N-cadherin-mediated contact inhibition of cell growth and S-phase entry

Oncogene. 1999 Jan 28;18(4):869-76. doi: 10.1038/sj.onc.1202396.


In this study the direct involvement of cadherins in adhesion-mediated growth inhibition was investigated. It is shown here that overexpression of N-cadherin in CHO cells significantly suppresses their growth rate. Interaction of these cells and two additional fibroblastic lines with synthetic beads coated with N-cadherin ligands (recombinant N-cadherin ectodomain or specific antibodies) leads to growth arrest at the G1 phase of the cell cycle. The cadherin-reactive beads inhibit the entry into S phase and the reduction in the levels of cyclin-dependent kinase (cdk) inhibitors p21 and p27, following serum-stimulation of starved cells. In exponentially growing cells these beads induce G1 arrest accompanied by elevation in p27 only. We propose that cadherin-mediated signaling is involved in contact inhibition of growth by inducing cell cycle arrest at the G1 phase and elevation of p27 levels.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CHO Cells
  • Cadherins / chemistry
  • Cadherins / genetics
  • Cadherins / metabolism*
  • Cell Communication*
  • Cell Count
  • Cell Cycle Proteins*
  • Cell Cycle* / drug effects
  • Cricetinae
  • Cyclin-Dependent Kinase Inhibitor p27
  • DNA, Complementary
  • G1 Phase
  • Ligands
  • Microtubule-Associated Proteins / metabolism*
  • Peptide Fragments / pharmacology
  • S Phase
  • Transfection
  • Tumor Suppressor Proteins*


  • Cadherins
  • Cell Cycle Proteins
  • DNA, Complementary
  • Ligands
  • Microtubule-Associated Proteins
  • Peptide Fragments
  • Tumor Suppressor Proteins
  • Cyclin-Dependent Kinase Inhibitor p27