Linked Life Data

11918080

Source:http://linkedlifedata.com/resource/pubmed/id/11918080

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-3-28
pubmed:abstractText
A previous study from our laboratory suggested that prostate cancer metastasis to bone may be mediated, in part, by preferential adhesion to human bone marrow endothelial (HBME) cells. Tumor cell adhesion to endothelial cells may be modulated by the effect of cytokines on cell adhesion molecules (CAMs). Tumor necrosis factor-alpha (TNF-alpha) regulates VCAM expression on the endothelium and this effect is enhanced by dihydrotestosterone (DHT). Transforming growth factor-beta (TGF-beta) stimulates the expression of alpha2beta1 integrin on PC-3 cells. The current study investigated the effects of the above cytokines and DHT (singularly and in various combinations) upon HBME and prostate cancer cell expression of VCAM, alpha2 integrin subunit, and beta1 integrin subunit by flow cytometry. We also monitored the effects of the above treatments on PC-3 cell adhesion to HBME monolayers. The data demonstrate that none of the treatments significantly altered the expression of selected CAMs on HBME cell and neoplastic prostate cell lines. The treatment of HBME monolayers with various combinations of cytokines and DHT prior to performing adhesion assays with PC-3 demonstrates that treatments containing TGF-beta reduced PC-3 cell adhesion to HBME monolayers by 32% or greater (P < 0.05). The reduction in PC-3 cell adhesion to TGF-beta-treated HBME monolayers was dose dependent. Interestingly, LNCaP cells but not PC-3 cells treated with TGF-beta had a reduced ability to adhere to untreated HBME monolayers. These results suggest that TGF-beta may reduce tumor cell adhesion to bone marrow microvascular endothelium, in vivo. The biological significance of this observation is discussed.
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
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
25-33
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11918080-Adenocarcinoma, pubmed-meshheading:11918080-Antigens, CD31, pubmed-meshheading:11918080-Bone Marrow, pubmed-meshheading:11918080-Cell Adhesion, pubmed-meshheading:11918080-Cell Adhesion Molecules, pubmed-meshheading:11918080-Cells, Cultured, pubmed-meshheading:11918080-Dihydrotestosterone, pubmed-meshheading:11918080-E-Selectin, pubmed-meshheading:11918080-Endothelium, Vascular, pubmed-meshheading:11918080-Flow Cytometry, pubmed-meshheading:11918080-Gene Expression Regulation, Neoplastic, pubmed-meshheading:11918080-Humans, pubmed-meshheading:11918080-Integrins, pubmed-meshheading:11918080-Male, pubmed-meshheading:11918080-Neoplasm Proteins, pubmed-meshheading:11918080-Prostatic Neoplasms, pubmed-meshheading:11918080-Receptors, Collagen, pubmed-meshheading:11918080-Transforming Growth Factor beta, pubmed-meshheading:11918080-Tumor Necrosis Factor-alpha, pubmed-meshheading:11918080-Vascular Cell Adhesion Molecule-1
pubmed:year
2002
pubmed:articleTitle
The regulation of prostate cancer cell adhesion to human bone marrow endothelial cell monolayers by androgen dihydrotestosterone and cytokines.
pubmed:affiliation
Department of Internal Medicine, University of Michigan Comprehensive Cancer Center, Ann Arbor 48109-0946, USA. cacooper@umich.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't