The Journal of Membrane Biology

, Volume 124, Issue 3, pp 207–225

Incorporation of the gene for a cell-cell channel protein into transformed cells leads to normalization of growth

  • Parmender P. Mehta
  • Agnes Hotz-Wagenblatt
  • Birgit Rose
  • David Shalloway
  • Warner R. Loewenstein
Articles

DOI: 10.1007/BF01994355

Cite this article as:
Mehta, P.P., Hotz-Wagenblatt, A., Rose, B. et al. J. Membrain Biol. (1991) 124: 207. doi:10.1007/BF01994355

Summary

Incorporation of the gene for connexin 43, a cell-cell channel protein of gap junction, into the genome of communication-deficient transformed mouse 10T1/2 cells restored junctional communication and inhibited growth. Growth was slowed, saturation density reduced and focus formation suppressed, and these effects were contingent on overexpression of the exogenous gene and the consequent enhancement of communication. In coculture with normal cells the growth of the connexin overexpressors was completely arrested, as these cells established strong communication with the normal ones. Thus, in culture by themselves or in coculture, the connexin overexpressor cells grew like normal cells. These results demonstrate that the cell-cell channel is instrumental in growth control; they are the expected behavior if the channel transmits cytoplasmic growth-regulatory signals.

Key Words

intercellular communicationgap junctionconnexingrowth controlcDNAconnexin43cell-cell channeljunctional communicationtransformationcancer etiology

Copyright information

© Springer-Verlag New York Inc. 1991

Authors and Affiliations

  • Parmender P. Mehta
    • 1
  • Agnes Hotz-Wagenblatt
    • 2
  • Birgit Rose
    • 1
  • David Shalloway
    • 2
  • Warner R. Loewenstein
    • 1
  1. 1.Department of Physiology and BiophysicsUniversity of Miami School of MedicineMiami
  2. 2.Section of Biochemistry, Molecular and Cell Biology and Department of PathologyCornell UniversityIthaca