Intercellular communication v& gap junctions may be an important mechanism of cellular growth control. Tumor promoters can inhibit intercellular communication between cultured cells, while genotoxic carcinogens apparently lack this capability. The inhibition of intercellular communication by tumor promoters may be an essential mechanism by which tumor promotion occurs in vivo.
In this study, the liver tumor promoters phenobarbital, lindane (1,2,3, 4,5, D D T (1,2,, Aroclor 1254 (a polychlorihated biphenyl mixture) and dieldrin inhibited intercellular communication between male B6C3 F1 mouse hepatocytes in primary culture. Intercellular communication was detected as the passage of [5-3 H]uridine nucleotides from pre-labelled donor hepatocytes to non-labelled recipient heptocytes. Mouse hepatocyte intercellular communication was also inhibited by the skin tumor promoter TPA (12-O-tetradecanoyl-phorbol-13-acetate), but not by the bladder tumor promoter saccharin. The genotoxic hepatocarcinogens dimethylnitrosamine, diethylnitrosamine, benzo [aj]gyrene and 2-acetylaminofluorene, and the hepatocytotoxins bromobenzene, acetaminophen, carbon tetrachloride, chloroform and methotrexate had no effect on mouse hepatocyte intercellular communication at non-cytotoxic levels. These results suggest that the ability to inhibit mouse hepatocyte intercellular communication is an effect specific to tumor promoters.