Regulation of T-cadherin by hormones, glucocorticoid and EGF

The cell adhesion molecule T-cadherin is an unusual member of the cadherin superfamily that lacks a cytoplasmic domain, binding instead to the cell membrane via a glycophosphatidyl inositol anchor. T-cadherin is a receptor for hexameric Acrp30/adiponectin and binds low-density lipoproteins in endoth...

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Bibliographic Details
Published in:Gene 2006-06, Vol.374, p.58-67
Main Authors: Bromhead, Collette, Miller, John H., McDonald, Fiona J.
Format: Article
Language:English
Subjects:
5' Flanking Region - genetics
Animals
Cadherins - genetics
Cadherins - metabolism
Cadherins - physiology
Cell adhesion
Cell Adhesion - drug effects
Cell Adhesion - physiology
Cell Line, Transformed
Cell Line, Tumor
Cell Transformation, Viral
Cercopithecus aethiops
COS Cells
Dexamethasone - pharmacology
Epidermal Growth Factor - pharmacology
Estradiol - pharmacology
Gene Expression Regulation - drug effects
Genes, Reporter
Glucocorticoids - pharmacology
H-cadherin
Hormones - pharmacology
Humans
Luciferases - metabolism
Osteoblasts
Osteosarcoma - pathology
Progesterone - pharmacology
Promoter
Promoter Regions, Genetic
Real-time RT-PCR
RNA, Messenger - analysis
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Summary:The cell adhesion molecule T-cadherin is an unusual member of the cadherin superfamily that lacks a cytoplasmic domain, binding instead to the cell membrane via a glycophosphatidyl inositol anchor. T-cadherin is a receptor for hexameric Acrp30/adiponectin and binds low-density lipoproteins in endothelial cells. T-cadherin is expressed widely in the brain and cardiovascular system, but expression is absent or decreased in several cancers. Little is known about the mechanisms and factors that control T-cadherin expression. Therefore, to investigate regulation of T-cadherin expression, we analysed 3.9 kb of the 5′-flanking region of human T-cadherin for promoter activity and identified potential transcription factor binding sites. Western blotting and a quantitative real-time RT-PCR assay developed for T-cadherin showed that estradiol, progesterone, EGF, dexamethasone and factors in serum were involved in transcriptional and post-transcriptional regulation of T-cadherin in human osteosarcoma cells; the effects observed were opposite to those described for T-cadherin's ligand, adiponectin. The data suggest that T-cadherin is regulated in a complex manner indicative of a role in hormone and drug-induced changes in bone morphology and pathology.
ISSN:0378-1119
1879-0038
DOI:10.1016/j.gene.2006.01.013