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E-cadherin, estrogens and cancer: is there a connection?
O W Blaschuk1, S B Munro, R Farookhi
1Department of Physiology, McGill University, Montreal, Quebec.
The Canadian Journal of Oncology
|November 1, 1994
Summary
E-cadherin, an epithelial cell adhesion molecule, acts as a tumor suppressor. Estrogens may increase cancer risk by decreasing E-cadherin levels in breast, uterine, and ovarian tissues.
Area of Science:
- Cell Biology
- Molecular Biology
- Oncology
Background:
- E-cadherin is a crucial calcium-dependent cell adhesion molecule in epithelial tissues.
- Emerging evidence suggests E-cadherin functions as a tumor suppressor.
- The cadherin superfamily plays vital roles in cellular structure and function.
Purpose of the Study:
- To review the structure, function, and regulation of E-cadherin and related cadherins.
- To examine the influence of estrogens on E-cadherin levels in vivo.
- To explore the hypothesis linking estrogen-induced E-cadherin down-regulation to specific cancers.
Main Methods:
- Literature review of existing studies on E-cadherin and cadherins.
- Analysis of research investigating estrogen's effects on E-cadherin expression.
- Synthesis of data to evaluate the proposed cancer promotion mechanism.
Main Results:
- E-cadherin's structure, function, and regulatory mechanisms are detailed.
- Studies demonstrate that estrogens can modulate E-cadherin levels.
- A correlation between estrogen exposure and reduced E-cadherin is observed in relevant tissues.
Conclusions:
- E-cadherin is a key regulator of epithelial integrity and a potential tumor suppressor.
- Estrogen's modulation of E-cadherin presents a plausible mechanism for promoting breast, uterine, and ovarian cancers.
- Further research is warranted to elucidate the precise role of E-cadherin in hormone-dependent carcinogenesis.