GAP JUNCTION FUNCTION AND CANCER

Abstract

Gap Junctions (GJs) provide cell-to-cell communication (GJIC) of essential metabolites and ions. Js allow tissues to average responses, clear waste products, and minimize the effects of xenobiotics by dilution and allowing steady-state catabolism. any chemicals can adversely affect the membrane GJ assembly causing reversible alterations in GJIC. uring toxicity essential metabolites, ions, and regulators are not shared homeostatically throughout a tissue community. lterations in metabolic circuits are thought to interrupt organ integration. ersistent GJ perturbation can cause chronic effects, e.g., cancer. any tumor promoters inhibit GJIC. iver precancerous foci cells intracommunicate (but at a reduced level), and intercommunicate improperly (or not at all) across the foci boundary to normal cells. In time, foci can become less regulated and more isolated within the tissue. Js remain reduced quantitatively in the progression stage and may be qualitatively altered in metastasis since connections are made between the primary tumor cells and foreign host calls at the secondary metastatic site. cell sorting and binding mechanisms by the cell adhesion molecules (CAM) and integrins may also be altered at secondary sites. his may allow the relocation of primary tumor cells and nurturance via GJs at the secondary site.

Citation

Holder, J., E. Elmore, AND J. Barrett. GAP JUNCTION FUNCTION AND CANCER. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-93/436 (NTIS PB94146248), 1993.

Additional Information

Cancer Research 53:3475-3485, 1993