Title: Chemical, oncogene and growth factor inhibition gap junctional intercellular communication: an integrative hypothesis of carcinogenesis.

Authors: Trosko, J E; Chang, C C; Madhukar, B V; Klaunig, J E

Published In Pathobiology, (1990)

Abstract: Most, if not all, cancer cells have some dysfunction in gap-junction-mediated intercellular communication, either because of defects in cell adhesion or inability to have functional gap junctional communication. In addition, most, if not all, tumor-promoting chemicals and conditions down-regulate gap junction function, while some antitumor-promoting chemicals can up-regulate gap junctional communication. Several oncogenes are associated with down-regulation of gap junction function and several hormone and growth regulators, known to be tumor promoters, are also able to down-regulate gap junction function. On the other hand, some tumor suppressor genes have been linked to the up-regulation of gap junctions. Based on these observations, it is hypothesized that, if a progenitor cell is unable to perform gap junctional intercellular communication, normal growth control and cell differentiation would not be possible, thereby favoring the development of malignant neoplasia.

PubMed ID: 2076190

MeSH Terms: Animals; Cell Communication/drug effects; Cell Communication/physiology; Growth Substances/physiology*; Humans; Intercellular Junctions/drug effects*; Intercellular Junctions/physiology; Neoplasms, Experimental/etiology*; Neoplasms, Experimental/pathology; Neoplasms, Experimental/physiopathology; Neoplasms/etiology*; Neoplasms/pathology; Neoplasms/physiopathology; Oncogenes/physiology*