The regulation of prostate cancer cell adhesion to human bone marrow endothelial cell monolayers by androgen dihydrotestosterone and cytokines
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 (CA...
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| Veröffentlicht in: | Clinical & experimental metastasis 2002, Vol.19 (1), p.25-33 |
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| creator | Cooper, Carlton R Bhatia, Jasmine K Muenchen, Heather J McLean, Lisa Hayasaka, Satoru Taylor, Jeremy Poncza, Paul J Pienta, Kenneth J |
| description | 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. |
| doi_str_mv | 10.1023/A:1013849123736 |
| format | Article |
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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.</description><identifier>ISSN: 0262-0898</identifier><identifier>EISSN: 1573-7276</identifier><identifier>DOI: 10.1023/A:1013849123736</identifier><identifier>PMID: 11918080</identifier><identifier>CODEN: CEXMD2</identifier><language>eng</language><publisher>Netherlands: Springer Nature B.V</publisher><subject>Adenocarcinoma - pathology ; Bone Marrow - blood supply ; Cell Adhesion - drug effects ; Cell Adhesion Molecules - biosynthesis ; Cell Adhesion Molecules - genetics ; Cells, Cultured ; Dihydrotestosterone - pharmacology ; E-Selectin - biosynthesis ; E-Selectin - genetics ; Endothelium, Vascular - cytology ; Flow Cytometry ; Gene Expression Regulation, Neoplastic - drug effects ; Humans ; Integrins - biosynthesis ; Integrins - genetics ; Male ; Neoplasm Proteins - metabolism ; Platelet Endothelial Cell Adhesion Molecule-1 - biosynthesis ; Platelet Endothelial Cell Adhesion Molecule-1 - genetics ; Prostatic Neoplasms - pathology ; Receptors, Collagen ; Transforming Growth Factor beta - pharmacology ; Tumor Necrosis Factor-alpha - pharmacology ; Vascular Cell Adhesion Molecule-1 - biosynthesis ; Vascular Cell Adhesion Molecule-1 - genetics</subject><ispartof>Clinical & experimental metastasis, 2002, Vol.19 (1), p.25-33</ispartof><rights>Copyright Kluwer Academic Publishers 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c280t-2545b94f7d35a0926a47b11f6b6a6ecd8e1998ae3755fed1e8e7f50ee8618d8e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,4010,27904,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11918080$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cooper, Carlton R</creatorcontrib><creatorcontrib>Bhatia, Jasmine K</creatorcontrib><creatorcontrib>Muenchen, Heather J</creatorcontrib><creatorcontrib>McLean, Lisa</creatorcontrib><creatorcontrib>Hayasaka, Satoru</creatorcontrib><creatorcontrib>Taylor, Jeremy</creatorcontrib><creatorcontrib>Poncza, Paul J</creatorcontrib><creatorcontrib>Pienta, Kenneth J</creatorcontrib><title>The regulation of prostate cancer cell adhesion to human bone marrow endothelial cell monolayers by androgen dihydrotestosterone and cytokines</title><title>Clinical & experimental metastasis</title><addtitle>Clin Exp Metastasis</addtitle><description>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.</description><subject>Adenocarcinoma - pathology</subject><subject>Bone Marrow - blood supply</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell Adhesion Molecules - biosynthesis</subject><subject>Cell Adhesion Molecules - genetics</subject><subject>Cells, Cultured</subject><subject>Dihydrotestosterone - pharmacology</subject><subject>E-Selectin - biosynthesis</subject><subject>E-Selectin - genetics</subject><subject>Endothelium, Vascular - cytology</subject><subject>Flow Cytometry</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Humans</subject><subject>Integrins - biosynthesis</subject><subject>Integrins - genetics</subject><subject>Male</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Platelet Endothelial Cell Adhesion Molecule-1 - biosynthesis</subject><subject>Platelet Endothelial Cell Adhesion Molecule-1 - genetics</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Receptors, Collagen</subject><subject>Transforming Growth Factor beta - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Vascular Cell Adhesion Molecule-1 - biosynthesis</subject><subject>Vascular Cell Adhesion Molecule-1 - genetics</subject><issn>0262-0898</issn><issn>1573-7276</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkE9P3DAQxS1UxG4XztwqqwduKR47_pPeECoFaaVe4Bw5yYSEJja1HVX5EnxmvFp66WlGej-9efMIuQT2DRgX1zffgYEwZQVcaKFOyBakFoXmWn0iW8YVL5ipzIZ8jvGFMVZqbc7IBqACwwzbkrfHAWnA52WyafSO-p6-Bh-TTUhb61oMtMVporYbMB6A5OmwzNbRxjuksw3B_6XoOp8GnEY7HfHZOz_ZFUOkzUqt64J_Rke7cVjzmjCmfAPDwSKLtF2T_z06jOfktLdTxIuPuSNPdz8eb--L_a-fD7c3-6LlhqWCy1I2VdnrTkjLKq5sqRuAXjXKKmw7g1BVxqLQUvbYARrUvWSIRoHJqtiRq6NvfvbPkuPU8xgPya1Dv8RagxRGcp7Br_-BL34JLmerOZSgOJcyQ18-oKWZsatfw5iLWet_NYt3s-CCTQ</recordid><startdate>2002</startdate><enddate>2002</enddate><creator>Cooper, Carlton R</creator><creator>Bhatia, Jasmine K</creator><creator>Muenchen, Heather J</creator><creator>McLean, Lisa</creator><creator>Hayasaka, Satoru</creator><creator>Taylor, Jeremy</creator><creator>Poncza, Paul J</creator><creator>Pienta, Kenneth J</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FG</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>P5Z</scope><scope>P62</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>2002</creationdate><title>The regulation of prostate cancer cell adhesion to human bone marrow endothelial cell monolayers by androgen dihydrotestosterone and cytokines</title><author>Cooper, Carlton R ; Bhatia, Jasmine K ; Muenchen, Heather J ; McLean, Lisa ; Hayasaka, Satoru ; Taylor, Jeremy ; Poncza, Paul J ; Pienta, Kenneth J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c280t-2545b94f7d35a0926a47b11f6b6a6ecd8e1998ae3755fed1e8e7f50ee8618d8e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adenocarcinoma - 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Academic</collection><jtitle>Clinical & experimental metastasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cooper, Carlton R</au><au>Bhatia, Jasmine K</au><au>Muenchen, Heather J</au><au>McLean, Lisa</au><au>Hayasaka, Satoru</au><au>Taylor, Jeremy</au><au>Poncza, Paul J</au><au>Pienta, Kenneth J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The regulation of prostate cancer cell adhesion to human bone marrow endothelial cell monolayers by androgen dihydrotestosterone and cytokines</atitle><jtitle>Clinical & experimental metastasis</jtitle><addtitle>Clin Exp Metastasis</addtitle><date>2002</date><risdate>2002</risdate><volume>19</volume><issue>1</issue><spage>25</spage><epage>33</epage><pages>25-33</pages><issn>0262-0898</issn><eissn>1573-7276</eissn><coden>CEXMD2</coden><abstract>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.</abstract><cop>Netherlands</cop><pub>Springer Nature B.V</pub><pmid>11918080</pmid><doi>10.1023/A:1013849123736</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma - pathology Bone Marrow - blood supply Cell Adhesion - drug effects Cell Adhesion Molecules - biosynthesis Cell Adhesion Molecules - genetics Cells, Cultured Dihydrotestosterone - pharmacology E-Selectin - biosynthesis E-Selectin - genetics Endothelium, Vascular - cytology Flow Cytometry Gene Expression Regulation, Neoplastic - drug effects Humans Integrins - biosynthesis Integrins - genetics Male Neoplasm Proteins - metabolism Platelet Endothelial Cell Adhesion Molecule-1 - biosynthesis Platelet Endothelial Cell Adhesion Molecule-1 - genetics Prostatic Neoplasms - pathology Receptors, Collagen Transforming Growth Factor beta - pharmacology Tumor Necrosis Factor-alpha - pharmacology Vascular Cell Adhesion Molecule-1 - biosynthesis Vascular Cell Adhesion Molecule-1 - genetics |
| title | The regulation of prostate cancer cell adhesion to human bone marrow endothelial cell monolayers by androgen dihydrotestosterone and cytokines |
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