ArticleBritish journal of cancer2001
Interactions of human prostatic epithelial cells with bone marrow endothelium: binding and invasion.
Article in British journal of cancer, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 81 citations in OpenAlex.
- Prostate cancer and bone: clinical presentation and molecular mechanisms.Endocrine-related cancer · 2023Review
- Non-canonical EphA2 activation underpins PTEN-mediated metastatic migration and poor clinical outcome in prostate cancer.British journal of cancer · 2022Article
- Review
- The TMEFF2 tumor suppressor modulates integrin expression, RhoA activation and migration of prostate cancer cells.Biochimica et biophysica acta · 2014Article
- Arachidonic acid induction of Rho-mediated transendothelial migration in prostate cancer.British journal of cancer · 2014Article
- Targeting constitutively activated β1 integrins inhibits prostate cancer metastasis.Molecular cancer research : MCR · 2013Article
- Definition of molecular determinants of prostate cancer cell bone extravasation.Cancer research · 2013Article
- Ligand-independent activation of EphA2 by arachidonic acid induces metastasis-like behaviour in prostate cancer cells.British journal of cancer · 2012Article
- The differential effects of statins on the metastatic behaviour of prostate cancer.British journal of cancer · 2012Article
- The chemokine receptor CX₃CR1 is directly involved in the arrest of breast cancer cells to the skeleton.Breast cancer research : BCR · 2011Article
- Steps in prostate cancer progression that lead to bone metastasis.International journal of cancer · 2011Review
- Article
- Individual rac GTPases mediate aspects of prostate cancer cell and bone marrow endothelial cell interactions.Journal of signal transduction · 2011Article
- N-acetylglucosamine: production and applications.Marine drugs · 2010Review
- Analysis of glycosyltransferase expression in metastatic prostate cancer cells capable of rolling activity on microvascular endothelial (E)-selectin.Glycobiology · 2008Article
- Stepping out of the flow: capillary extravasation in cancer metastasis.Clinical & experimental metastasis · 2008Review
- Hypoxia and the presence of human vascular endothelial cells affect prostate cancer cell invasion and metabolism.Neoplasia (New York, N.Y.) · 2007Article
- Targeting selectins and selectin ligands in inflammation and cancer.Expert opinion on therapeutic targets · 2007Review
- Human cytomegalovirus infection alters PC3 prostate carcinoma cell adhesion to endothelial cells and extracellular matrix.Neoplasia (New York, N.Y.) · 2006Article
- Bone microenvironment modulates expression and activity of cathepsin B in prostate cancer.Neoplasia (New York, N.Y.) · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer shows a propensity to form secondary tumours within the bone marrow. Such tumours are the major cause of mortality in this disease. We have developed an in vitro system to study the binding of prostate epithelial cells to bone marrow endothelium (BME) and stroma (BMS). The metastatic prostate cancer cell line, PC3 (derived from a bone metastasis), was seeded onto confluent layers of BME and its binding characteristics compared to human umbilical vein endothelial cells (HUVEC), lung endothelium (Hs888Lu) and BMS. The PC3 cell line showed significantly increased binding to BME (P< 0.05) compared to endothelium derived from HUVEC and lung or BMS with maximal binding occurring at 1 h. Following pre-incubation with a beta1 integrin antibody PC3 binding to BME was inhibited by 64% (P< 0.001). Antibodies directed against the integrins beta4, alpha2, alpha4, alpha5 and the cellular adhesion molecules P-selectin, CD31, VCAM-1 and sialy Lewis X showed no effect on blocking PC3 binding. Primary prostatic epithelial cells from both malignant (n = 11) and non-malignant tissue (n = 11) also demonstrated equivalent levels of increased adhesion to BME and BMS compared to HUVEC, peaking at 24 h. Further studies examined the invasive ability of prostate epithelial cells in response to bone marrow endothelium using Matrigel invasion chamber assays. In contrast to the previous results, malignant cells showed an increase (1000 fold) in invasive ability, whilst non-malignant prostate epithelia did not respond. We have shown that both malignant and non-malignant prostate epithelial cells can bind at equivalent levels and preferentially to primary human bone marrow endothelium in comparison to controls. However, only malignant prostate epithelia show increased invasive ability in response to BME.
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