PMID- 11918080
OWN - NLM
STAT- MEDLINE
DCOM- 20020422
LR  - 20191025
IS  - 0262-0898 (Print)
IS  - 0262-0898 (Linking)
VI  - 19
IP  - 1
DP  - 2002
TI  - The regulation of prostate cancer cell adhesion to human bone marrow endothelial 
      cell monolayers by androgen dihydrotestosterone and cytokines.
PG  - 25-33
AB  - 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.
FAU - Cooper, Carlton R
AU  - Cooper CR
AD  - Department of Internal Medicine, University of Michigan Comprehensive Cancer 
      Center, Ann Arbor 48109-0946, USA. cacooper@umich.edu
FAU - Bhatia, Jasmine K
AU  - Bhatia JK
FAU - Muenchen, Heather J
AU  - Muenchen HJ
FAU - McLean, Lisa
AU  - McLean L
FAU - Hayasaka, Satoru
AU  - Hayasaka S
FAU - Taylor, Jeremy
AU  - Taylor J
FAU - Poncza, Paul J
AU  - Poncza PJ
FAU - Pienta, Kenneth J
AU  - Pienta KJ
LA  - eng
GR  - CA 46592/CA/NCI NIH HHS/United States
GR  - P50 CA 69568/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Clin Exp Metastasis
JT  - Clinical & experimental metastasis
JID - 8409970
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (E-Selectin)
RN  - 0 (Integrins)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Platelet Endothelial Cell Adhesion Molecule-1)
RN  - 0 (Receptors, Collagen)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 08J2K08A3Y (Dihydrotestosterone)
SB  - IM
MH  - Adenocarcinoma/*pathology
MH  - Bone Marrow/*blood supply
MH  - Cell Adhesion/*drug effects
MH  - Cell Adhesion Molecules/biosynthesis/genetics
MH  - Cells, Cultured
MH  - Dihydrotestosterone/*pharmacology
MH  - E-Selectin/biosynthesis/genetics
MH  - Endothelium, Vascular/*cytology
MH  - Flow Cytometry
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Humans
MH  - Integrins/biosynthesis/genetics
MH  - Male
MH  - Neoplasm Proteins/metabolism
MH  - Platelet Endothelial Cell Adhesion Molecule-1/biosynthesis/genetics
MH  - Prostatic Neoplasms/*pathology
MH  - Receptors, Collagen
MH  - Transforming Growth Factor beta/*pharmacology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Vascular Cell Adhesion Molecule-1/biosynthesis/genetics
EDAT- 2002/03/29 10:00
MHDA- 2002/04/23 10:01
CRDT- 2002/03/29 10:00
PHST- 2002/03/29 10:00 [pubmed]
PHST- 2002/04/23 10:01 [medline]
PHST- 2002/03/29 10:00 [entrez]
AID - 10.1023/a:1013849123736 [doi]
PST - ppublish
SO  - Clin Exp Metastasis. 2002;19(1):25-33. doi: 10.1023/a:1013849123736.