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Critical Reviews™ in Oncogenesis
SJR: 0.631 SNIP: 0.503 CiteScore™: 2

ISSN Print: 0893-9675
ISSN Online: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.v12.i3-4.30
pages 225-256

Downregulation of Gap Junctions in Cancer Cells

Edward Leithe
Department of Cancer Prevention, Institute for Cancer Research, Rikshospitalet-Radiumhospitalet Medical Center, 0310 Oslo, Norway
Solveig Sirnes
Department of Cancer Prevention, Institute for Cancer Research, Rikshospitalet-Radiumhospitalet Medical Center, 0310 Oslo, Norway
Yasufumi Omori
Department of Pathology, Akita University School of Medicine, Akita, 010-8543, Japan
Edgar Rivedal
Department of Cancer Prevention, Institute for Cancer Research, Rikshospitalet-Radiumhospitalet Medical Center, 0310 Oslo, Norway

ABSTRACT

Gap junctions are intercellular plasma membrane domains enriched in channels that allow direct exchange of ions and small molecules between adjacent cells. Gap junction channels are composed of a family of transmembrane proteins called connexin. Connexins play important roles in the regulation of cell growth and differentiation. Cancer cells usually have downregulated levels of gap junctions, and several lines of evidence suggest that loss of gap junctional intercellular communication is an important step in carcinogenesis. In support of this hypothesis are studies showing that reexpression of connexins in cancer cells causes normalization of cell growth control and reduced tumor growth. To gain a more detailed understanding of the role of connexins as tumor suppressors, a clearer picture of the mechanisms involved in loss of gap junctions in cancer cells is needed. Furthermore, defining the mechanisms involved in downregulation of connexins in carcinogenesis will be an important step toward utilizing the potential of connexins as targets in cancer prevention and therapy. Various mechanisms are involved in the loss of gap junctions in cancer cells, ranging from loss of connexin gene transcription to aberrant trafficking of connexin proteins. This review will discuss our current knowledge on the molecular mechanisms involved in the downregulation of gap junctions in cancer cells.


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