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Defective E-cadherin/catenin complexes in human cancer
E Van Aken1, O De Wever, A S Correia da Rocha
1Department of Ophthalmology, Ghent University Hospital, Gent, Belgium.
Abstract:
Cancer is caused by a series of genomic changes leading directly or indirectly to disturbance of growth, differentiation and tissue integrity. Genomic, transcriptional or posttranscriptional alterations of E-cadherin/catenin complexes that are implicated in various steps of cancer development comprise mutational inactivation, transcriptional downregulation of E-cadherin sometimes accompanied by upregulation of N-cadherin, proteolysis of E-cadherin and posttranslational stabilisation of beta-catenin and plakoglobin. The E-cadherin/catenin complex serves not only cell-cell adhesion but also transduces signals to the nucleus and to the cytoskeleton, either directly or through its connections with multiple other complexes. We review here the expression of E-cadherin/catenin in human cancers, emphasising methods of observation and prognostic interpretation of results. This is illustrated in thyroid lesions from the benign follicular adenoma to the extremely malignant anaplastic carcinoma. The eye is an organ largely neglected by students of cadherins and catenins. The implication of a variety of members of these molecular families in the embryonic development of the eye strongly suggests that disturbances of cadherin/catenin complexes are crucial also in the development of ocular tumours.
Insights
Cancer involves genomic changes affecting cell adhesion. Alterations in E-cadherin/catenin complexes are key in cancer development and progression, impacting cell-cell adhesion and signaling.
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- Cancer arises from genomic alterations disrupting normal cellular processes.
- E-cadherin/catenin complexes are crucial for cell-cell adhesion and signal transduction.
- Dysregulation of these complexes is implicated in various stages of cancer development.
Purpose of the Study:
- To review the expression of E-cadherin/catenin in human cancers.
- To emphasize methods for observing and interpreting these complexes prognostically.
- To explore their role in thyroid and ocular tumors.
Main Methods:
- Review of existing literature on E-cadherin/catenin expression in human cancers.
- Analysis of expression patterns in thyroid lesions (benign to malignant).
- Discussion of implications in ocular tumor development.
Main Results:
- Genomic, transcriptional, and posttranscriptional alterations of E-cadherin/catenin complexes are common in cancer.
- These alterations include inactivation, downregulation, proteolysis, and stabilization of key proteins.
- Expression patterns vary across cancer types, with prognostic significance.
Conclusions:
- E-cadherin/catenin complexes are critical in cancer pathogenesis.
- Their altered expression and function contribute to tumor development and progression.
- Further research into their role in ocular tumors is warranted.