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Connexins as precocious markers and molecular targets for chemical and pharmacological agents in carcinogenesis
G Pointis1, C Fiorini, J Gilleron
1INSERM U 670, Faculté de Médecine, 27 avenue de Valombrose, 06107 Nice cedex 02, France. pointis@unice.fr
Abstract:
Gap junctions, intercellular channels structured by the connexin protein family, have been implicated in the control of cell homeostasis, proliferation, differentiation and death. A loss of the gap junction intercellular communication and/or connexin dysfunction are typical features of cancer per se and have been associated with the effect of many carcinogens. Indeed, many early human neoplasia of various organs and human tumor cell lines exhibit deficient connexin-mediated communication expression mainly related, in a large number of observations, with an aberrant cytoplasmic localization of this membranous protein. Restoration of normal phenotype in transformed cells by restoration of exogenous connexin gave rise to the concept that connexins may act as tumor suppressors. However, the mechanisms by which connexins mediate such a tumor suppressor effect are multiple. They may result from: formation of functional channels; hemichannels or are directly associated with connexin expression. In addition, the literature shows that they may be dependent upon the cell type and the connexin type. In the present review, we analyze all these aspects of connexin/gap junction involvement in the carcinogenesis process, in human cancers and discuss the possibility of using connexins as potential anti-oncogenic targets for cancer chemoprevention and/or chemotherapy.
Insights
Gap junctions, formed by connexins, regulate cell functions. Loss of gap junction communication is linked to cancer, suggesting connexins may act as tumor suppressors.
Area of Science:
- Cell biology
- Oncology
- Molecular biology
Background:
- Gap junctions, formed by connexins, are crucial for cell communication and homeostasis.
- Dysfunctional gap junctions and connexin loss are hallmarks of cancer, often linked to carcinogen exposure.
- Aberrant cytoplasmic localization of connexins is frequently observed in human neoplasia.
Purpose of the Study:
- To review the role of connexins and gap junctions in carcinogenesis.
- To explore the tumor suppressor functions of connexins.
- To discuss connexins as potential targets for cancer chemoprevention and chemotherapy.
Main Methods:
- Literature review of studies on gap junctions, connexins, and cancer.
- Analysis of connexin involvement in cell homeostasis, proliferation, differentiation, and death.
- Examination of connexin mechanisms in tumor suppression, including channel formation and direct effects.
Main Results:
- Connexin dysfunction and loss of gap junction communication are associated with various human cancers.
- Restoring connexin expression can reverse the transformed phenotype, supporting their tumor suppressor role.
- Connexin-mediated tumor suppression mechanisms are diverse and cell/connexin type-dependent.
Conclusions:
- Connexins play a significant role in cancer development and progression.
- Connexins exhibit tumor suppressor activities through multiple mechanisms.
- Targeting connexins offers potential for novel cancer chemoprevention and chemotherapy strategies.
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