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

Research output: Contribution to journalArticle

172 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)207-225
Number of pages19
JournalThe Journal of Membrane Biology
Volume124
Issue number3
DOIs
Publication statusPublished - Dec 1 1991

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Keywords

  • cDNA
  • cancer etiology
  • cell-cell channel
  • connexin
  • connexin43
  • gap junction
  • growth control
  • intercellular communication
  • junctional communication
  • transformation

ASJC Scopus subject areas

  • Biophysics
  • Physiology
  • Cell Biology

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