Linked Life Data

18563594

Source:http://linkedlifedata.com/resource/pubmed/id/18563594

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2008-10-6
pubmed:abstractText
Stromal derived factor-1 (SDF-1 or CXCL12) expressed by osteoblasts and endothelial cells, and its receptors CXCR4 and CXCR7/RDC1 are key molecular determinants in prostate cancer (PCa) metastasis. What drives PCa cells into the extravascular marrow space(s) once they make contact with the blood vessel endothelium, however remains unclear. Here, we evaluated whether degradation of CXCL12 facilitates PCa cell entry into the marrow cavity by locally lowering CXCL12 levels intravascularly. To explore this possibility, co-cultured conditioned media from PCa cells and endothelial cells were evaluated for their ability to degrade biotinylated CXCL12 (bCXCL12). Co-culture of PCa cells/endothelial cells resulted in greater digestion of CXCL12 than was achieved by either cell type alone, and this activity regulated invasion in vitro. The ability to degrade CXCL12 was not however observed in PCa and osteoblasts co-cultures. Fractionation and inhibitor studies suggested that the activity was CD26/dipeptidyl peptidase IV (DPPIV) and possibly other cysteine/serine proteases. By inhibiting CD26/DPPIV, invasion and metastasis of PCa cell lines were enhanced in in vitro and in vivo metastasis assays. Together, these data suggest that the degradation of CXCL12 by CD26/DPPIV may be involved in the metastatic cascades of PCa, and suggests that inhibition of CD26/DPPIV may be a trigger of PCa metastasis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0262-0898
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
765-76
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
CD26/dipeptidyl peptidase IV regulates prostate cancer metastasis by degrading SDF-1/CXCL12.
pubmed:affiliation
Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Room 3307, 1011 North University Avenue, Ann Arbor, MI 48109-1078, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural