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Intercellular communication and carcinogenesis

H Yamasaki¹, M Mesnil, Y Omori

¹Unit of Multistage Carcinogenesis, International Agency for Research on Cancer, Lyon, France.

Mutation Research

|December 1, 1995

Summary

Aberrant gap junctional intercellular communication (GJIC) is linked to cancer. Certain connexin genes, crucial for GJIC, function as tumor suppressors, suggesting their role in cancer prevention.

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Area of Science:

Cell Biology
Molecular Biology
Cancer Research

Background:

Intercellular communication, both humoral and cell contact-mediated, regulates cellular functions.
Aberrant humoral communication is linked to carcinogenesis, with growth factors and receptors identified as oncogenes.
Cell contact-mediated communication, particularly gap junctional intercellular communication (GJIC), plays a critical role in carcinogenesis and cell growth control.

Purpose of the Study:

To investigate the role of GJIC in carcinogenesis.
To explore molecular mechanisms underlying aberrant GJIC in cancer.
To determine if connexin genes function as tumor suppressors.

Main Methods:

In vivo studies on rat liver exposed to tumor-promoting agents.

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Analysis of molecular mechanisms of aberrant GJIC, including gene mutation, mRNA expression, protein localization, and functional modulation.

Transfection studies of connexin genes into tumor cells.

Main Results:

Liver tumor-promoting agents were shown to inhibit GJIC in vivo.
Aberrant connexin protein localization was identified as a common mechanism in cancer cells, potentially involving altered phosphorylation and lack of cell adhesion.
While connexin gene mutations may be rare, some mutations (e.g., cx 37) were reported in a mouse lung tumor cell line.

Conclusions:

Aberrant GJIC is implicated in cancer development.
Connexin genes, such as cx 26, cx 43, and cx 32, exhibit tumor-suppressor properties.
Understanding aberrant GJIC mechanisms is crucial for cancer research and potential therapeutic strategies.