Growth inhibition of transformed cells correlates with their junctional communication with normal cells.
The growth of various chemically and virally transformed cell types in culture is inhibited when they are in contact with normal cell types. We show that this growth inhibition is contingent on the presence of junctional communication between the normal and transformed cells (heterologous communication), as probed with a 443 dalton microinjected fluorescent tracer. In cell combinations where heterologous communication is weak or absent there is no detectable growth inhibition; the inhibition appears when communication is induced by cyclic AMP-dependent phosphorylation, and only then. In cell combinations where heterologous communication is spontaneously strong, the growth inhibition is present, but it is abolished when the communication is blocked by retinol or retinoic acid. The cell-to-cell membrane channels of gap junctions are the likely conduits of the signals for this growth control.
P P
PP
Mehta
J S
JS
Bertram
W R
WR
Loewenstein
D012368:4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone / Q000494:pharmacology; D000818:Animals; D003411:Arvicolinae; D002450:Cell Communication; D002471:Cell Transformation, Neoplastic / Q000139:chemically induced / Q000187:drug effects / Q000503:physiopathology*; D005576:Colforsin / Q000494:pharmacology; D003260:Contact Inhibition; D000242:Cyclic AMP / Q000502:physiology; D007365:Intercellular Junctions / Q000502:physiology*; D007473:Ion Channels / Q000502:physiology; D051379:Mice; D051381:Rats; D014212:Tretinoin / Q000494:pharmacology; D014801:Vitamin A / Q000494:pharmacology; D014970:Xanthines / Q000494:pharmacology
D007473:Ion Channels; D014970:Xanthines; D014801:Vitamin A; D005576:Colforsin; C008514:methylxanthine; D012368:4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone; D014212:Tretinoin; D000242:Cyclic AMP