α-Chemokine growth factors for adenocarcinomas; a synthetic peptide inhibitor for α-chemokines inhibits the growth of adenocarcinoma cell lines

The experiments aimed to determine if alpha-chemokine inhibitors are effective suppressors of the growth of adenocarcinomas, a neoplasm with a high mortality rate. Expression of growth-related oncogene (GROalpha) and interleukin-8 (IL-8) was determined by enzyme-linked immunosorbent assay. Inhibitio...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of cancer research and clinical oncology 2000-01, Vol.126 (1), p.19-26
Hauptverfasser: FUJISAWA, N, SAKAO, Y, HAYASHI, S, HADDEN, W. A, HARMON, C. L, MILLER, E. J
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 26
container_issue 1
container_start_page 19
container_title Journal of cancer research and clinical oncology
container_volume 126
creator FUJISAWA, N
SAKAO, Y
HAYASHI, S
HADDEN, W. A
HARMON, C. L
MILLER, E. J
description The experiments aimed to determine if alpha-chemokine inhibitors are effective suppressors of the growth of adenocarcinomas, a neoplasm with a high mortality rate. Expression of growth-related oncogene (GROalpha) and interleukin-8 (IL-8) was determined by enzyme-linked immunosorbent assay. Inhibition of alpha-chemokine binding to tumor cells was assessed in the presence and absence of the hexapeptide, antileukinate. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays were performed to determine the effect of alpha-chemokines, monoclonal antibodies (mAb), and antileukinate on cell proliferation. Finally, antileukinate inhibition of human, lung adenocarcinoma tumor growth, was determined in BALB/c nude mice. All of the adenocarcinomas tested produced either GROalpha or IL-8 or both. Proliferation of lung, stomach and colon adenocarcinoma cells was inhibited by anti-GROalpha mAb and/or anti-IL-8 mAb while recombinant human GROalpha stimulated the proliferation of lung and stomach adenocarcinomas. Antileukinate inhibited GROalpha binding to specific receptors on adenocarcinoma cells and inhibited the proliferation of all adenocarcinomas tested. Colon-derived adenocarcinomas specifically bound IL-8 and this binding was also inhibited by antileukinate. Administration of antileukinate in vivo inhibited the tumor growth of adenocarcinoma A549. GROalpha and IL-8 are necessary for the growth of lung, stomach and colon adenocarcinomas, and can be inhibited by the hexapeptide, antileukinate. The findings suggest the possibility of using alpha-chemokine receptor inhibitors in the treatment of adenocarcinoma.
doi_str_mv 10.1007/PL00008460
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_70903643</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>70903643</sourcerecordid><originalsourceid>FETCH-LOGICAL-c312t-95a3381e65a3030e4dae993e1e817300f2726cf05fe87a3507b3c3d1408fc7233</originalsourceid><addsrcrecordid>eNpdkd9KwzAUxoMobk5vfADJhXghVE-atunwSob_YKAXel2y9MRG22YmHbLH8FF8EZ_J1G0oBsIhnN_3nXA-Qg4ZnDEAcf4whXDyJIMtMmQJjyPGebpNhsAEi9KYZQOy5_0LhHcq4l0yYJAlTCTpkHx8fUaTChv7alqkz86-dxXVUnXWeaqto7LE1irplGltI_0FldQv267Czig6x3lnSqSmrczMBM2PJFiqjaXf9DwNms0Aq__5UoV1TetesE92tKw9HqzriDxdXz1ObqPp_c3d5HIaKc7iLhqnkvOcYRYqcMCklDgec2SYM8EBdCziTGlINeZC8hTEjCtesgRyrUTM-YicrHznzr4t0HdFY3z_DdmiXfhCwBh4lvTg6QpUznrvUBdzZxrplgWDog-g-A0gwEdr18WswfIPutp4AI7XgPRK1trJVhn_y8Uhv3C_AVfJkDw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>70903643</pqid></control><display><type>article</type><title>α-Chemokine growth factors for adenocarcinomas; a synthetic peptide inhibitor for α-chemokines inhibits the growth of adenocarcinoma cell lines</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>FUJISAWA, N ; SAKAO, Y ; HAYASHI, S ; HADDEN, W. A ; HARMON, C. L ; MILLER, E. J</creator><creatorcontrib>FUJISAWA, N ; SAKAO, Y ; HAYASHI, S ; HADDEN, W. A ; HARMON, C. L ; MILLER, E. J</creatorcontrib><description>The experiments aimed to determine if alpha-chemokine inhibitors are effective suppressors of the growth of adenocarcinomas, a neoplasm with a high mortality rate. Expression of growth-related oncogene (GROalpha) and interleukin-8 (IL-8) was determined by enzyme-linked immunosorbent assay. Inhibition of alpha-chemokine binding to tumor cells was assessed in the presence and absence of the hexapeptide, antileukinate. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays were performed to determine the effect of alpha-chemokines, monoclonal antibodies (mAb), and antileukinate on cell proliferation. Finally, antileukinate inhibition of human, lung adenocarcinoma tumor growth, was determined in BALB/c nude mice. All of the adenocarcinomas tested produced either GROalpha or IL-8 or both. Proliferation of lung, stomach and colon adenocarcinoma cells was inhibited by anti-GROalpha mAb and/or anti-IL-8 mAb while recombinant human GROalpha stimulated the proliferation of lung and stomach adenocarcinomas. Antileukinate inhibited GROalpha binding to specific receptors on adenocarcinoma cells and inhibited the proliferation of all adenocarcinomas tested. Colon-derived adenocarcinomas specifically bound IL-8 and this binding was also inhibited by antileukinate. Administration of antileukinate in vivo inhibited the tumor growth of adenocarcinoma A549. GROalpha and IL-8 are necessary for the growth of lung, stomach and colon adenocarcinomas, and can be inhibited by the hexapeptide, antileukinate. The findings suggest the possibility of using alpha-chemokine receptor inhibitors in the treatment of adenocarcinoma.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/PL00008460</identifier><identifier>PMID: 10641745</identifier><identifier>CODEN: JCROD7</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Adenocarcinoma - drug therapy ; Adenocarcinoma - metabolism ; Animals ; Antineoplastic agents ; Biological and medical sciences ; Chemokine CXCL1 ; Chemokines, CXC - antagonists &amp; inhibitors ; Chemokines, CXC - metabolism ; Chemotactic Factors - metabolism ; Enzyme-Linked Immunosorbent Assay ; General aspects ; Growth Inhibitors - pharmacology ; Growth Substances - metabolism ; Humans ; Intercellular Signaling Peptides and Proteins ; Interleukin-8 - metabolism ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Neoplasm Proteins - pharmacology ; Oligopeptides - pharmacology ; Pharmacology. Drug treatments ; Proto-Oncogenes - drug effects ; Tumor Cells, Cultured</subject><ispartof>Journal of cancer research and clinical oncology, 2000-01, Vol.126 (1), p.19-26</ispartof><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c312t-95a3381e65a3030e4dae993e1e817300f2726cf05fe87a3507b3c3d1408fc7233</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=1243224$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10641745$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FUJISAWA, N</creatorcontrib><creatorcontrib>SAKAO, Y</creatorcontrib><creatorcontrib>HAYASHI, S</creatorcontrib><creatorcontrib>HADDEN, W. A</creatorcontrib><creatorcontrib>HARMON, C. L</creatorcontrib><creatorcontrib>MILLER, E. J</creatorcontrib><title>α-Chemokine growth factors for adenocarcinomas; a synthetic peptide inhibitor for α-chemokines inhibits the growth of adenocarcinoma cell lines</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><description>The experiments aimed to determine if alpha-chemokine inhibitors are effective suppressors of the growth of adenocarcinomas, a neoplasm with a high mortality rate. Expression of growth-related oncogene (GROalpha) and interleukin-8 (IL-8) was determined by enzyme-linked immunosorbent assay. Inhibition of alpha-chemokine binding to tumor cells was assessed in the presence and absence of the hexapeptide, antileukinate. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays were performed to determine the effect of alpha-chemokines, monoclonal antibodies (mAb), and antileukinate on cell proliferation. Finally, antileukinate inhibition of human, lung adenocarcinoma tumor growth, was determined in BALB/c nude mice. All of the adenocarcinomas tested produced either GROalpha or IL-8 or both. Proliferation of lung, stomach and colon adenocarcinoma cells was inhibited by anti-GROalpha mAb and/or anti-IL-8 mAb while recombinant human GROalpha stimulated the proliferation of lung and stomach adenocarcinomas. Antileukinate inhibited GROalpha binding to specific receptors on adenocarcinoma cells and inhibited the proliferation of all adenocarcinomas tested. Colon-derived adenocarcinomas specifically bound IL-8 and this binding was also inhibited by antileukinate. Administration of antileukinate in vivo inhibited the tumor growth of adenocarcinoma A549. GROalpha and IL-8 are necessary for the growth of lung, stomach and colon adenocarcinomas, and can be inhibited by the hexapeptide, antileukinate. The findings suggest the possibility of using alpha-chemokine receptor inhibitors in the treatment of adenocarcinoma.</description><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma - metabolism</subject><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Chemokine CXCL1</subject><subject>Chemokines, CXC - antagonists &amp; inhibitors</subject><subject>Chemokines, CXC - metabolism</subject><subject>Chemotactic Factors - metabolism</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>General aspects</subject><subject>Growth Inhibitors - pharmacology</subject><subject>Growth Substances - metabolism</subject><subject>Humans</subject><subject>Intercellular Signaling Peptides and Proteins</subject><subject>Interleukin-8 - metabolism</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Neoplasm Proteins - pharmacology</subject><subject>Oligopeptides - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Proto-Oncogenes - drug effects</subject><subject>Tumor Cells, Cultured</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkd9KwzAUxoMobk5vfADJhXghVE-atunwSob_YKAXel2y9MRG22YmHbLH8FF8EZ_J1G0oBsIhnN_3nXA-Qg4ZnDEAcf4whXDyJIMtMmQJjyPGebpNhsAEi9KYZQOy5_0LhHcq4l0yYJAlTCTpkHx8fUaTChv7alqkz86-dxXVUnXWeaqto7LE1irplGltI_0FldQv267Czig6x3lnSqSmrczMBM2PJFiqjaXf9DwNms0Aq__5UoV1TetesE92tKw9HqzriDxdXz1ObqPp_c3d5HIaKc7iLhqnkvOcYRYqcMCklDgec2SYM8EBdCziTGlINeZC8hTEjCtesgRyrUTM-YicrHznzr4t0HdFY3z_DdmiXfhCwBh4lvTg6QpUznrvUBdzZxrplgWDog-g-A0gwEdr18WswfIPutp4AI7XgPRK1trJVhn_y8Uhv3C_AVfJkDw</recordid><startdate>20000101</startdate><enddate>20000101</enddate><creator>FUJISAWA, N</creator><creator>SAKAO, Y</creator><creator>HAYASHI, S</creator><creator>HADDEN, W. A</creator><creator>HARMON, C. L</creator><creator>MILLER, E. J</creator><general>Springer</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20000101</creationdate><title>α-Chemokine growth factors for adenocarcinomas; a synthetic peptide inhibitor for α-chemokines inhibits the growth of adenocarcinoma cell lines</title><author>FUJISAWA, N ; SAKAO, Y ; HAYASHI, S ; HADDEN, W. A ; HARMON, C. L ; MILLER, E. J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c312t-95a3381e65a3030e4dae993e1e817300f2726cf05fe87a3507b3c3d1408fc7233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma - metabolism</topic><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Chemokine CXCL1</topic><topic>Chemokines, CXC - antagonists &amp; inhibitors</topic><topic>Chemokines, CXC - metabolism</topic><topic>Chemotactic Factors - metabolism</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>General aspects</topic><topic>Growth Inhibitors - pharmacology</topic><topic>Growth Substances - metabolism</topic><topic>Humans</topic><topic>Intercellular Signaling Peptides and Proteins</topic><topic>Interleukin-8 - metabolism</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Neoplasm Proteins - pharmacology</topic><topic>Oligopeptides - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Proto-Oncogenes - drug effects</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FUJISAWA, N</creatorcontrib><creatorcontrib>SAKAO, Y</creatorcontrib><creatorcontrib>HAYASHI, S</creatorcontrib><creatorcontrib>HADDEN, W. A</creatorcontrib><creatorcontrib>HARMON, C. L</creatorcontrib><creatorcontrib>MILLER, E. J</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cancer research and clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FUJISAWA, N</au><au>SAKAO, Y</au><au>HAYASHI, S</au><au>HADDEN, W. A</au><au>HARMON, C. L</au><au>MILLER, E. J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>α-Chemokine growth factors for adenocarcinomas; a synthetic peptide inhibitor for α-chemokines inhibits the growth of adenocarcinoma cell lines</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2000-01-01</date><risdate>2000</risdate><volume>126</volume><issue>1</issue><spage>19</spage><epage>26</epage><pages>19-26</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><coden>JCROD7</coden><abstract>The experiments aimed to determine if alpha-chemokine inhibitors are effective suppressors of the growth of adenocarcinomas, a neoplasm with a high mortality rate. Expression of growth-related oncogene (GROalpha) and interleukin-8 (IL-8) was determined by enzyme-linked immunosorbent assay. Inhibition of alpha-chemokine binding to tumor cells was assessed in the presence and absence of the hexapeptide, antileukinate. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays were performed to determine the effect of alpha-chemokines, monoclonal antibodies (mAb), and antileukinate on cell proliferation. Finally, antileukinate inhibition of human, lung adenocarcinoma tumor growth, was determined in BALB/c nude mice. All of the adenocarcinomas tested produced either GROalpha or IL-8 or both. Proliferation of lung, stomach and colon adenocarcinoma cells was inhibited by anti-GROalpha mAb and/or anti-IL-8 mAb while recombinant human GROalpha stimulated the proliferation of lung and stomach adenocarcinomas. Antileukinate inhibited GROalpha binding to specific receptors on adenocarcinoma cells and inhibited the proliferation of all adenocarcinomas tested. Colon-derived adenocarcinomas specifically bound IL-8 and this binding was also inhibited by antileukinate. Administration of antileukinate in vivo inhibited the tumor growth of adenocarcinoma A549. GROalpha and IL-8 are necessary for the growth of lung, stomach and colon adenocarcinomas, and can be inhibited by the hexapeptide, antileukinate. The findings suggest the possibility of using alpha-chemokine receptor inhibitors in the treatment of adenocarcinoma.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>10641745</pmid><doi>10.1007/PL00008460</doi><tpages>8</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0171-5216
ispartof Journal of cancer research and clinical oncology, 2000-01, Vol.126 (1), p.19-26
issn 0171-5216
1432-1335
language eng
recordid cdi_proquest_miscellaneous_70903643
source MEDLINE; SpringerLink Journals - AutoHoldings
subjects Adenocarcinoma - drug therapy
Adenocarcinoma - metabolism
Animals
Antineoplastic agents
Biological and medical sciences
Chemokine CXCL1
Chemokines, CXC - antagonists & inhibitors
Chemokines, CXC - metabolism
Chemotactic Factors - metabolism
Enzyme-Linked Immunosorbent Assay
General aspects
Growth Inhibitors - pharmacology
Growth Substances - metabolism
Humans
Intercellular Signaling Peptides and Proteins
Interleukin-8 - metabolism
Medical sciences
Mice
Mice, Inbred BALB C
Neoplasm Proteins - pharmacology
Oligopeptides - pharmacology
Pharmacology. Drug treatments
Proto-Oncogenes - drug effects
Tumor Cells, Cultured
title α-Chemokine growth factors for adenocarcinomas; a synthetic peptide inhibitor for α-chemokines inhibits the growth of adenocarcinoma cell lines
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-24T23%3A52%3A27IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=%CE%B1-Chemokine%20growth%20factors%20for%20adenocarcinomas;%20a%20synthetic%20peptide%20inhibitor%20for%20%CE%B1-chemokines%20inhibits%20the%20growth%20of%20adenocarcinoma%20cell%20lines&rft.jtitle=Journal%20of%20cancer%20research%20and%20clinical%20oncology&rft.au=FUJISAWA,%20N&rft.date=2000-01-01&rft.volume=126&rft.issue=1&rft.spage=19&rft.epage=26&rft.pages=19-26&rft.issn=0171-5216&rft.eissn=1432-1335&rft.coden=JCROD7&rft_id=info:doi/10.1007/PL00008460&rft_dat=%3Cproquest_cross%3E70903643%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=70903643&rft_id=info:pmid/10641745&rfr_iscdi=true