Chemical Tumor Promoters, Oncogenes and Growth Factors: Modulators of Gap Junctional Intercellular Communication

Abstract

Gap junctional intercellular communication has been linked to the regulation of cell proliferation and differentiation. Since most normal mammalian cells have functional gap junctions while most malignant cells do not, it has been hypothesized that the carcinogenic process involves the inhibition of this important biological process. Using several in vitro assays (metabolic cooperation; Fluorescent Recovery After Photobleaching of FRAP ; scrape loading dye transfer; and the cell mat assay), we have examined the effects of various oncogenes, chemical tumor promoters, and growth factors on gap junction function. Natural products (phorbolesters, teleocidin), drugs (phenobarbital), food additives (saccharin), solvents (heptanol), pollutants (PCBs, PBBs), pesticides and herbicides (DDT, 2,3,5-T), nutritional factors (unsaturated fatty acids), growth factors (EGF, TGF-B), metabolic byproducts (H202, cholesterol epoxides), oncogenes (src, ras), cigarette tar condensates, heavy metals (mercuric chloride), neurotoxins (dieldrin) and neurotransmitters (acetylcholine) have been shown to modulate gap junctional communication.

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Document Details

Document Type
Technical Report
Publication Date
Jan 01, 1991
Accession Number
ADA246766

Entities

People

  • James E. Trosko

Organizations

  • Michigan State University

Tags

Communities of Interest

  • Materials and Manufacturing Processes

DTIC Thesaurus Topics

  • Air Force
  • Cell Membrane
  • Cell Physiological Processes
  • Cells
  • Cellular Structures
  • Epithelial Cells
  • Fatty Acids
  • Growth Factors
  • Intercellular Junctions
  • Modulators
  • Molecules
  • Neoplasms
  • Peptide Growth Factors
  • Proteins
  • Small Molecules
  • Stem Cells

Fields of Study

  • Chemistry

Readers

  • Aquatic Ecology
  • Molecular Biology and Genetics
  • Toxicology/Environmental Toxicology