Two major alterations in gap junctional intercellular communication (GJIC) during experimental carcinogenesis have been seen: a decrease of its capacity during tumor promotion and a selective loss of intercellular communication between transformed cells and surrounding normal counterparts. These data, first discovered in our laboratory on mouse fibroblasts (BALB/c 3T3), were partly confirmed in rat liver epithelial cells. In such cells, the decreased GJIC was related to their level of transformation. Tissue-specific effect of tumor promoters is also seen in the inhibition of GJIC; administration of phenobarbital decreased the level of GJ mRNA in the liver, but not in other organs tested. Phenobarbital also inhibited GJIC among adult rat hepatocytes co-cultured with BALB/c 3T3 cells but not among the mouse fibroblasts. Moreover, our findings on the diminished level of GJ mRNA in tumors of rat liver support the importance of acquired selective GJIC in rat liver carcinogenesis.
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