| dc.contributor.author | WAN, H | en_US |
| dc.date.accessioned | 2016-11-15T15:24:05Z | |
| dc.date.available | 2015-01-16 | en_US |
| dc.date.issued | 2015-01-21 | en_US |
| dc.date.submitted | 2016-11-08T16:05:04.794Z | |
| dc.identifier.issn | 2072-6694 | en_US |
| dc.identifier.uri | http://qmro.qmul.ac.uk/xmlui/handle/123456789/17653 | |
| dc.description.abstract | Desmoglein 3 is one of seven desmosomal cadherins that mediate cell-cell adhesion in desmosomes. Desmosomes are the intercellular junctional complexes that anchor the intermediate filaments of adjacent cells and confer strong cell adhesion thus are essential in the maintenance of tissue architecture and structural integrity. Like adherens junctions, desmosomes function as tumour suppressors and are down regulated in the process of epithelial-mesenchymal transition and in tumour cell invasion and metastasis. However, recently several studies have shown that various desmosomal components, including desmoglein 3, are up-regulated in cancer with increased levels of expression correlating with the clinical stage of malignancy, implicating their potentiality to serve as a diagnostic and prognostic marker. Furthermore, in vitro studies have demonstrated that overexpression of desmoglein 3 in cancer cell lines activates several signal pathways that have an impact on cell morphology, adhesion and locomotion. These additional signalling roles of desmoglein 3 may not be associated to its adhesive function in desmosomes but rather function outside of the junctions, acting as a key regulator in the control of actin based cellular processes. This review will discuss recent advances which support the role of desmoglein 3 in cancer progression. | en_US |
| dc.description.sponsorship | The authors would like to thank Medical Research Council, British Skin Foundation and Institute of
Dentistry, School of Medicine and Dentistry, Queen Mary University of London for support to the work
in the authors’ lab. | en_US |
| dc.format.extent | 266 - 286 (21) | en_US |
| dc.language | English | en_US |
| dc.publisher | MDPI | en_US |
| dc.relation.ispartof | Cancers | en_US |
| dc.rights | This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/). | |
| dc.title | Desmoglein 3: a help or a hindrance in cancer progression? | en_US |
| dc.type | Article | |
| dc.rights.holder | © 2015 by the authors; licensee MDPI, Basel, Switzerland | |
| dc.identifier.doi | 10.3390/cancers7010266 | en_US |
| pubs.author-url | http://www.dentistry.qmul.ac.uk/staff/drhongwan.html | en_US |
| pubs.issue | 7 | en_US |
| pubs.notes | Not known | en_US |
| pubs.notes | Desmoglein 3 is found to be up-regulated in cancer only in the last 10 years or so and its role in tumour cell biology remains not fully understood. This article provides the first overview of recent advances on the role of Desmoglein 3 in cancer in the literature. | en_US |
| pubs.publication-status | Published | en_US |
| pubs.publisher-url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4381258/ | en_US |
| pubs.volume | Cancers 2015 | en_US |
| dcterms.dateAccepted | 2015-01-16 | en_US |
