Incorporation of the gene for a cell-cell channel protein into transformed cells leads to normalization of growth |
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Authors: | Parmender P. Mehta Agnes Hotz-Wagenblatt Birgit Rose David Shalloway Warner R. Loewenstein |
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Affiliation: | (1) Department of Physiology and Biophysics, University of Miami School of Medicine, 33136 Miami, Florida;(2) Section of Biochemistry, Molecular and Cell Biology and Department of Pathology, Cornell University, 14853 Ithaca, New York |
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Abstract: | 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. |
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Keywords: | intercellular communication gap junction connexin growth control cDNA connexin43 cell-cell channel junctional communication transformation cancer etiology |
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