Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-4-3
pubmed:abstractText
DMBT1 and galectin-3 are potential interacting proteins with presumably complex roles in tumorigenesis. While at present a variety of mechanisms are discussed for DMBT1 and its participation in cancer, galectin-3 is commonly known to exert tumor-promoting effects. However, in vitro studies in a rodent system have suggested that DMBT1/galectin-3 interaction in the ECM triggers epithelial differentiation, which would point to tumor-suppressive properties. To improve the understanding of DMBT1/galectin-3 action in cancer, we carried out studies in skin cancer of different origins. Mutational analyses of DMBT1 identified a missense mutation in 1 of 13 melanoma cell lines. It led to an exchange of an evolutionary conserved proline residue for serine and located within the second CUB domain of DMBT1. Immunohistochemical analyses demonstrated absence of DMBT1/galectin-3 expression from melanocytes but induction of DMBT1 expression in 1 of 8 nevi and 1 of 11 melanomas and of galectin-3 expression in 3 of 8 nevi and 4 of 8 melanomas. These data suggest that DMBT1 and galectin-3 are unlikely to act as classical tumor suppressors in melanomas. DMBT1 and galectin-3 appear to be secreted to the ECM by epithelial cells within the epidermis and the hair follicle. Compared to the flanking normal epidermis, skin tumors of epithelial origin frequently displayed downregulation of DMBT1 (18 of 19 cases) and galectin-3 (12 of 12 cases). Thus, loss of DMBT1/galectin-3 expression may play a role in the genesis of epithelial skin cancer. This would support the view that galectin-3 can exert tumor-suppressive effects in certain scenarios, and DMBT1/galectin-3-mediated differentiation represents a candidate mechanism for this effect.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0020-7136
pubmed:author
pubmed:copyrightInfo
Copyright 2003 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
105
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
149-57
pubmed:dateRevised
2007-7-24
pubmed:meshHeading
pubmed-meshheading:12673672-Agglutinins, pubmed-meshheading:12673672-Carcinoma, Basal Cell, pubmed-meshheading:12673672-Carcinoma, Squamous Cell, pubmed-meshheading:12673672-Case-Control Studies, pubmed-meshheading:12673672-Chromosomes, Human, Pair 10, pubmed-meshheading:12673672-DNA Mutational Analysis, pubmed-meshheading:12673672-DNA Primers, pubmed-meshheading:12673672-Down-Regulation, pubmed-meshheading:12673672-Galectin 3, pubmed-meshheading:12673672-Gene Expression Regulation, Neoplastic, pubmed-meshheading:12673672-Genes, Tumor Suppressor, pubmed-meshheading:12673672-Humans, pubmed-meshheading:12673672-Immunoenzyme Techniques, pubmed-meshheading:12673672-Loss of Heterozygosity, pubmed-meshheading:12673672-Melanocytes, pubmed-meshheading:12673672-Melanoma, pubmed-meshheading:12673672-Microsatellite Repeats, pubmed-meshheading:12673672-Polymerase Chain Reaction, pubmed-meshheading:12673672-Receptors, Cell Surface, pubmed-meshheading:12673672-Skin Neoplasms, pubmed-meshheading:12673672-Tumor Cells, Cultured
pubmed:year
2003
pubmed:articleTitle
Frequent downregulation of DMBT1 and galectin-3 in epithelial skin cancer.
pubmed:affiliation
Department of Molecular Genome Analysis, Deutsches Krebsforschungszentrum, Heidelberg, Germany. j.mollenhauer@dfkz.de
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't