Soluble E-cadherin: more than a symptom of disease
- PMID: 22201848
- PMCID: PMC4183062
- DOI: 10.2741/4031
Soluble E-cadherin: more than a symptom of disease
Abstract
Epithelial (E)-cadherin is a homophilic adhesion molecule which is responsible for maintenance of baso-lateral cell adhesion and polarity. E-cadherin can be lost from the cell surface by proteolytic cleavage, resulting in the generation of an 80kDa fragment referred to a soluble E-cadherin (sE-cad). Although originally discovered in the conditioned media of breast cancer cells and later verified in the fluids of cancer patients, today sE-cad has been reported in patients with viral and bacterial infections, organ failure, and benign disease. The proteases implicated in this cleavage event include members of the disintegrin family (ADAM10 and 15), bacterial proteases (gingipains and BFT), cathepsins (B, L, S), matrix metalloproteases (MMP-2, 3, 7, 9, and 14), Kallikrein-7 (KLK7), and plasmin. Stimulus that induces sE-cad generation by ADAMs, MMPs, KLK7, and plasmin in vitro ranges from serum withdrawal to pro-inflammatory cytokines to growth factors. The cellular or physiologic consequences of sE-cad accumulation include the disruption of adherens junctions, cellular migration and invasion, induction of MMPs, as well as cell signaling, suggesting that sE-cad may contribute to disease progression.
Figures
References
-
- Grundemann Carsten, Bauer Monika, Schweier Oliver, von Oppen Nanette, Lassing Ute, Saudan Philippe, Becker Karl-Friedrich, Karp Klaus, Hanke Thomas, Bachmann Martin F. Hanspeter Pircher: Cutting Edge: Identification of E-Cadherin as a Ligand for the Murine Killer Cell Lectin-Like Receptor G1. The Journal of Immunology. 2006;176(3):1311–1315. - PubMed
-
- Ito Masayuki, Maruyama Takuma, Saito Naotoshi, Koganei Satoru, Yamamoto Kazuo, Matsumoto Naoki. Killer cell lectin-like receptor G1 binds three members of the classical cadherin family to inhibit NK cell cytotoxicity. The Journal of Experimental Medicine. 2006;203(2):289–295. doi: 10.1084/jem.20051986. - DOI - PMC - PubMed
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Miscellaneous
