Inhibition of hepatocyte gap junctional intercellular communication by tumor promoters.

摘要

he mechanisms by which tumor promoters enhance neoplasia are poorly understood. One effect common to most tumor promoters is thier ability to inhibit the cell-to-cell exchange of small molecules and ions through gap junctions, i.e., gap junctional intercellular communication (IC). IC may be necessary for normal growth control and the loss of IC may predispose cells to enhanced growth. In the present studies, the effects of liver tumor promoters and other agents on IC between rodent hepatocytes in primary culture has been studied. IC was detected between hepatocytes: (1) autoradiographically following the passage and incorporation of (5-