Journal
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
Volume 1826, Issue 1, Pages 23-31Publisher
ELSEVIER
DOI: 10.1016/j.bbcan.2012.03.002
Keywords
E-cadherin; Epithelial-mesenchymal transition; Mesenchymal-epithelial transition; Oncogene; Tumorigenesis; Adherens junctions
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Funding
- NCI NIH HHS [P50 CA108961-07, R01 CA100467-05, R01 CA100467, P50 CA108961] Funding Source: Medline
- NINDS NIH HHS [R01 NS069753-02, R01 NS069753] Funding Source: Medline
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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. (C) 2012 Elsevier B.V. All rights reserved.
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