Journal
FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 17, Issue -, Pages 1948-1964Publisher
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/4031
Keywords
Soluble E-cadherin; ADAM; MMP; Cancer; Disease; Biomarker; Review
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Funding
- NATIONAL CANCER INSTITUTE [T32CA009676, R01CA154252] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007315] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA154252, T32 CA009676] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007315] Funding Source: Medline
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Epithelial (E)-cadherin is a homophilic adhesion molecule which is responsible for maintenance of basolateral 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.
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