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Connexins and cancer.

¹Equipe Communications Jonctionnelles, Laboratoire des Biomembranes et Signalisation Cellulaire, CNRS-UMR 6558, Université de Poitiers, 40, Avenue du Recteur Pineau, 86022 cedex, Poitiers, France. marc.mesnil@univ-poitiers.fr

Biology of the Cell

|February 5, 2003

Summary

Reduced gap junction communication, crucial for cell growth control, is frequently observed in cancer. Loss of connexin function actively contributes to carcinogenesis by promoting tumor growth and hindering normal cell interactions.

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Area of Science:

Cell Biology
Oncology
Molecular Biology

Background:

Gap junctional intercellular communication (GJIC) has been hypothesized to play a role in carcinogenesis for decades.
Decreased or absent GJIC is a common observation in cells exposed to tumor promoters, transformed cells, and between tumor and normal cells across various species and tissues.
Connexins (Cx), the proteins forming gap junctions, have been identified as potential tumor suppressors, further supporting their role in cancer development.

Purpose of the Study:

To review the historical perspective and accumulated evidence on the role of GJIC in carcinogenesis.
To discuss the proposed mechanisms by which inhibited GJIC contributes to tumor promotion and progression.
To highlight the current knowledge gaps regarding the molecular regulation by GJIC and its specific involvement in human cancers.

Main Methods:

Literature review and historical analysis of research on GJIC and cancer.
In vitro and in vivo experimental models to study GJIC in various cell types and conditions.
Analysis of data linking connexin function and tumor suppression.

Main Results:

Consistent evidence shows reduced GJIC in various cancer models and with tumor-promoting agents.
Inhibition of GJIC is implicated in two key stages of carcinogenesis: tumor promotion and post-transformation progression.
Connexins' tumor-suppressive properties and their role in reverting transformed cell phenotypes are increasingly recognized.

Conclusions:

The historical data strongly support the involvement of GJIC dysfunction in carcinogenesis.
Further research is needed to elucidate the precise molecular mechanisms regulated by GJIC and to investigate its role in human cancers.
Understanding connexin function and GJIC is critical for developing novel cancer prevention and therapeutic strategies.

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