Abstract
In the context of cancer, E-cadherin has traditionally been categorized as a tumor suppressor, given its essential role in the formation of proper intercellular junctions, and its downregulation in the process of epithelial-mesenchymal transition (EMT) in epithelial tumor progression. Germline or somatic mutations in the E-cadherin gene (. CDH1) or downregulation by epigenetic mechanisms have been described in a small subset of epithelial cancers. However, recent evidence also points toward a promoting role of E-cadherin in several aspects of tumor progression. This includes preserved (or increased) E-cadherin expression in microemboli of inflammatory breast carcinoma, a possible "mesenchymal to epithelial transition" (MET) in ovarian carcinoma, collective cell invasion in some epithelial cancers, a recent association of E-cadherin expression with a more aggressive brain tumor subset, as well as the intriguing possibility of E-cadherin involvement in specific signaling networks in the cytoplasm and/or nucleus. In this review we address a lesser-known, positive role for E-cadherin in cancer.
Original language | English (US) |
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Pages (from-to) | 23-31 |
Number of pages | 9 |
Journal | Biochimica et Biophysica Acta - Reviews on Cancer |
Volume | 1826 |
Issue number | 1 |
DOIs | |
State | Published - Aug 2012 |
Externally published | Yes |
Keywords
- Adherens junctions
- E-cadherin
- Epithelial-mesenchymal transition
- Mesenchymal-epithelial transition
- Oncogene
- Tumorigenesis
ASJC Scopus subject areas
- Oncology
- Genetics
- Cancer Research