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Gap junctions and cancer: communicating for 50 years

Nature Reviews Cancer volume 16, pages 775788 (2016) | Download Citation

  • A Corrigendum to this article was published on 02 December 2016

This article has been updated

Abstract

Fifty years ago, tumour cells were found to lack electrical coupling, leading to the hypothesis that loss of direct intercellular communication is commonly associated with cancer onset and progression. Subsequent studies linked this phenomenon to gap junctions composed of connexin proteins. Although many studies support the notion that connexins are tumour suppressors, recent evidence suggests that, in some tumour types, they may facilitate specific stages of tumour progression through both junctional and non-junctional signalling pathways. This Timeline article highlights the milestones connecting gap junctions to cancer, and underscores important unanswered questions, controversies and therapeutic opportunities in the field.

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Change history

  • 02 December 2016

    On page 779 of the above article there were errors in line 7 of Table 1. The carcinogen used in the mouse model was DEN and the outcome was increased liver tumours in males only. This has now been corrected in the online version.

  • 26 October 2016

    In the original version of this article published online the DOI number was incorrect. This error has been corrected in the HTML and PDF versions of the article.

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Acknowledgements

Given that there are more than 1,500 papers dealing with connexins and cancer, the authors apologize to authors whose work was not cited in this review. Work in the authors' laboratories is supported by; Instituto de Salud Carlos III grant PI13/00763 and CP10/00624, co-financed by the European Regional Development Fund (ERDF) to T.A., Ligue contre le cancer (Comités de Charente, de Charente-maritime, des Deux-Sèvres, du Morbihan et de la Vienne) to M.M., US National Institutes of Health grant GM55632 to P.D.L., Canadian Institutes of Health Research, Canadian Cancer Society and Canada Research Chairs Program to C.C.N. and Canadian Institutes of Health Research (130530; 123228), Canadian Cancer Society (701459) and Canada Research Chair Program to D.W.L.

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Affiliations

  1. Translational Molecular Pathology, Vall d'Hebron Institute of Research, Barcelona 08035, Spain.

    • Trond Aasen
  2. STIM Laboratory ERL 7368 CNRS – Faculté des Sciences Fondamentales et Appliquées, Université de Poitiers, Poitiers 86073, France.

    • Marc Mesnil
  3. the Department of Cellular and Physiological Sciences, The Life Sciences Institute, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada.

    • Christian C. Naus
  4. Translational Research Program, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.

    • Paul D. Lampe
  5. Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario N6A 5C1, Canada.

    • Dale W. Laird

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Competing interests

The authors declare no competing financial interests.

Corresponding authors

Correspondence to Trond Aasen or Dale W. Laird.

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  1. 1.

    Supplementary information S1 (figure)

    The extended Cx43 interactome.

  2. 2.

    Supplementary information S2 (table)

    The extended Cx43 interactome retrieved and constructed using the STRING database version 10.0 (http://string-db.org), using a high confidence score prediction setting (>0.7) as viewed in Supplementary Information S1. In bold are hits from the highest prediction setting of (>0.9) as viewed in Figure 4.

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https://doi.org/10.1038/nrc.2016.105

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