The colony-stimulating factor-1 (CSF-1) receptor sustains ERK1/2 activation and proliferation in breast cancer cell lines
Breast cancer is the second leading cause of cancer-related deaths in western countries. Colony-Stimulating Factor-1 (CSF-1) and its receptor (CSF-1R) regulate macrophage and osteoclast production, trophoblast implantation and mammary gland development. The expression of CSF-1R and/or CSF-1 strongly...
Gespeichert in:
| Veröffentlicht in: | PloS one 2011-11, Vol.6 (11), p.e27450-e27450 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e27450 |
|---|---|
| container_issue | 11 |
| container_start_page | e27450 |
| container_title | PloS one |
| container_volume | 6 |
| creator | Morandi, Andrea Barbetti, Valentina Riverso, Maria Dello Sbarba, Persio Rovida, Elisabetta |
| description | Breast cancer is the second leading cause of cancer-related deaths in western countries. Colony-Stimulating Factor-1 (CSF-1) and its receptor (CSF-1R) regulate macrophage and osteoclast production, trophoblast implantation and mammary gland development. The expression of CSF-1R and/or CSF-1 strongly correlates with poor prognosis in several human epithelial tumors, including breast carcinomas. We demonstrate that CSF-1 and CSF-1R are expressed, although at different levels, in 16/17 breast cancer cell lines tested with no differences among molecular subtypes. The role of CSF-1/CSF-1R in the proliferation of breast cancer cells was then studied in MDAMB468 and SKBR3 cells belonging to different subtypes. CSF-1 administration induced ERK1/2 phosphorylation and enhanced cell proliferation in both cell lines. Furthermore, the inhibition of CSF-1/CSF-1R signaling, by CSF-1R siRNA or imatinib treatment, impaired CSF-1 induced ERK1/2 activation and cell proliferation. We also demonstrate that c-Jun, cyclin D1 and c-Myc, known for their involvement in cell proliferation, are downstream CSF-1R in breast cancer cells. The presence of a proliferative CSF-1/CSF-1R autocrine loop involving ERK1/2 was also found. The wide expression of the CSF-1/CSF-1R pair across breast cancer cell subtypes supports CSF-1/CSF-1R targeting in breast cancer therapy. |
| doi_str_mv | 10.1371/journal.pone.0027450 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1311931894</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A476863270</galeid><doaj_id>oai_doaj_org_article_52c43650751740078d22c5593aa5f1b2</doaj_id><sourcerecordid>A476863270</sourcerecordid><originalsourceid>FETCH-LOGICAL-c658t-978a12f9aa7f3342781795c6a8b06acd477527f7266d95d00e81feb14613ac1b3</originalsourceid><addsrcrecordid>eNptUltrFDEYHUSxtfoPRAM-qA-zzWWSzLwIZWm1WBC0PodvMsk2JZusyUxh_71Zd1q6UvKQcHLO-S6cqnpL8IIwSU5v45QC-MUmBrPAmMqG42fVMekYrQXF7Pmj91H1KudbjDlrhXhZHVGKO8Flc1xtr28M0tHHsK3z6NaTh9GFFbKgx5hqgj4tf13U5DNKRptNgVCe8gguZHT-8zs5pagQ3V0RxYAgDGiTonfWpD3iAuqTgTwiDUGbhLTxHnkXTH5dvbDgs3kz3yfV74vz6-W3-urH18vl2VWtBW_HupMtEGo7AGkZa6hsiey4FtD2WIAeGik5lVZSIYaODxiblljTk0YQBpr07KR6v_fd-JjVvLWsCCNlPaTtmsK43DOGCLdqk9wa0lZFcOofENNKQRqd9kZxqhsmOJacyAZj2Q6Uas47BsAt6Wnx-jJXm_q1GbQJYwJ_YHr4E9yNWsU7xSihXMhi8HE2SPHPZPKo1i7vtgbBxCmrDhcWpgQX5of_mE8PN7NWUPp3wcZSVu881VkjRSsYlTuvxROscgazdrokzLqCHwiavUCnmHMy9mFEgtUun_fNqF0-1ZzPInv3eD0PovtAsr-VHOB9</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1311931894</pqid></control><display><type>article</type><title>The colony-stimulating factor-1 (CSF-1) receptor sustains ERK1/2 activation and proliferation in breast cancer cell lines</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Public Library of Science (PLoS) Journals Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Morandi, Andrea ; Barbetti, Valentina ; Riverso, Maria ; Dello Sbarba, Persio ; Rovida, Elisabetta</creator><contributor>Ulasov, Ilya</contributor><creatorcontrib>Morandi, Andrea ; Barbetti, Valentina ; Riverso, Maria ; Dello Sbarba, Persio ; Rovida, Elisabetta ; Ulasov, Ilya</creatorcontrib><description>Breast cancer is the second leading cause of cancer-related deaths in western countries. Colony-Stimulating Factor-1 (CSF-1) and its receptor (CSF-1R) regulate macrophage and osteoclast production, trophoblast implantation and mammary gland development. The expression of CSF-1R and/or CSF-1 strongly correlates with poor prognosis in several human epithelial tumors, including breast carcinomas. We demonstrate that CSF-1 and CSF-1R are expressed, although at different levels, in 16/17 breast cancer cell lines tested with no differences among molecular subtypes. The role of CSF-1/CSF-1R in the proliferation of breast cancer cells was then studied in MDAMB468 and SKBR3 cells belonging to different subtypes. CSF-1 administration induced ERK1/2 phosphorylation and enhanced cell proliferation in both cell lines. Furthermore, the inhibition of CSF-1/CSF-1R signaling, by CSF-1R siRNA or imatinib treatment, impaired CSF-1 induced ERK1/2 activation and cell proliferation. We also demonstrate that c-Jun, cyclin D1 and c-Myc, known for their involvement in cell proliferation, are downstream CSF-1R in breast cancer cells. The presence of a proliferative CSF-1/CSF-1R autocrine loop involving ERK1/2 was also found. The wide expression of the CSF-1/CSF-1R pair across breast cancer cell subtypes supports CSF-1/CSF-1R targeting in breast cancer therapy.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0027450</identifier><identifier>PMID: 22096574</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Apoptosis ; Autocrine signalling ; Benzamides ; Binding sites ; Biocompatibility ; Biology ; Biomedical materials ; Biotechnology ; Blotting, Western ; Breast cancer ; Breast carcinoma ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; c-Jun protein ; c-Myc protein ; Cancer ; Cancer research ; Cancer therapies ; Cell activation ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - drug effects ; Colonies ; Colony-stimulating factor ; Cyclin D1 ; Electrophoresis, Polyacrylamide Gel ; Enzyme-Linked Immunosorbent Assay ; Extracellular signal-regulated kinase ; Fibroblasts ; Flow Cytometry ; Gene expression ; Genomes ; Health aspects ; Hep G2 Cells ; Humans ; Imatinib ; Imatinib Mesylate ; Immunoblotting ; Implantation ; Kinases ; Laboratories ; Ligands ; Macrophage colony stimulating factor ; Macrophage Colony-Stimulating Factor - metabolism ; Macrophage Colony-Stimulating Factor - pharmacology ; Macrophages ; Mammary gland ; Medical prognosis ; Medical research ; Medicine ; Metabolism ; Mice ; Mitogen-Activated Protein Kinase 1 - genetics ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - genetics ; Mitogen-Activated Protein Kinase 3 - metabolism ; Mutation ; Myc protein ; NIH 3T3 Cells ; Phosphorylation ; Phosphorylation - drug effects ; Piperazines - pharmacology ; Prognosis ; Pyrimidines - pharmacology ; Real-Time Polymerase Chain Reaction ; Receptor, Macrophage Colony-Stimulating Factor - genetics ; Receptor, Macrophage Colony-Stimulating Factor - metabolism ; RNA, Small Interfering - genetics ; Signal transduction ; siRNA ; Transcription factors ; Transgenic animals ; Tumor cell lines ; Tumorigenesis ; Tumors</subject><ispartof>PloS one, 2011-11, Vol.6 (11), p.e27450-e27450</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Morandi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Morandi et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c658t-978a12f9aa7f3342781795c6a8b06acd477527f7266d95d00e81feb14613ac1b3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3212567/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3212567/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79472,79473</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22096574$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Ulasov, Ilya</contributor><creatorcontrib>Morandi, Andrea</creatorcontrib><creatorcontrib>Barbetti, Valentina</creatorcontrib><creatorcontrib>Riverso, Maria</creatorcontrib><creatorcontrib>Dello Sbarba, Persio</creatorcontrib><creatorcontrib>Rovida, Elisabetta</creatorcontrib><title>The colony-stimulating factor-1 (CSF-1) receptor sustains ERK1/2 activation and proliferation in breast cancer cell lines</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Breast cancer is the second leading cause of cancer-related deaths in western countries. Colony-Stimulating Factor-1 (CSF-1) and its receptor (CSF-1R) regulate macrophage and osteoclast production, trophoblast implantation and mammary gland development. The expression of CSF-1R and/or CSF-1 strongly correlates with poor prognosis in several human epithelial tumors, including breast carcinomas. We demonstrate that CSF-1 and CSF-1R are expressed, although at different levels, in 16/17 breast cancer cell lines tested with no differences among molecular subtypes. The role of CSF-1/CSF-1R in the proliferation of breast cancer cells was then studied in MDAMB468 and SKBR3 cells belonging to different subtypes. CSF-1 administration induced ERK1/2 phosphorylation and enhanced cell proliferation in both cell lines. Furthermore, the inhibition of CSF-1/CSF-1R signaling, by CSF-1R siRNA or imatinib treatment, impaired CSF-1 induced ERK1/2 activation and cell proliferation. We also demonstrate that c-Jun, cyclin D1 and c-Myc, known for their involvement in cell proliferation, are downstream CSF-1R in breast cancer cells. The presence of a proliferative CSF-1/CSF-1R autocrine loop involving ERK1/2 was also found. The wide expression of the CSF-1/CSF-1R pair across breast cancer cell subtypes supports CSF-1/CSF-1R targeting in breast cancer therapy.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Autocrine signalling</subject><subject>Benzamides</subject><subject>Binding sites</subject><subject>Biocompatibility</subject><subject>Biology</subject><subject>Biomedical materials</subject><subject>Biotechnology</subject><subject>Blotting, Western</subject><subject>Breast cancer</subject><subject>Breast carcinoma</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>c-Jun protein</subject><subject>c-Myc protein</subject><subject>Cancer</subject><subject>Cancer research</subject><subject>Cancer therapies</subject><subject>Cell activation</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Colonies</subject><subject>Colony-stimulating factor</subject><subject>Cyclin D1</subject><subject>Electrophoresis, Polyacrylamide Gel</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Extracellular signal-regulated kinase</subject><subject>Fibroblasts</subject><subject>Flow Cytometry</subject><subject>Gene expression</subject><subject>Genomes</subject><subject>Health aspects</subject><subject>Hep G2 Cells</subject><subject>Humans</subject><subject>Imatinib</subject><subject>Imatinib Mesylate</subject><subject>Immunoblotting</subject><subject>Implantation</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Ligands</subject><subject>Macrophage colony stimulating factor</subject><subject>Macrophage Colony-Stimulating Factor - metabolism</subject><subject>Macrophage Colony-Stimulating Factor - pharmacology</subject><subject>Macrophages</subject><subject>Mammary gland</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mitogen-Activated Protein Kinase 1 - genetics</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - genetics</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Mutation</subject><subject>Myc protein</subject><subject>NIH 3T3 Cells</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Piperazines - pharmacology</subject><subject>Prognosis</subject><subject>Pyrimidines - pharmacology</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Receptor, Macrophage Colony-Stimulating Factor - genetics</subject><subject>Receptor, Macrophage Colony-Stimulating Factor - metabolism</subject><subject>RNA, Small Interfering - genetics</subject><subject>Signal transduction</subject><subject>siRNA</subject><subject>Transcription factors</subject><subject>Transgenic animals</subject><subject>Tumor cell lines</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</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><sourceid>DOA</sourceid><recordid>eNptUltrFDEYHUSxtfoPRAM-qA-zzWWSzLwIZWm1WBC0PodvMsk2JZusyUxh_71Zd1q6UvKQcHLO-S6cqnpL8IIwSU5v45QC-MUmBrPAmMqG42fVMekYrQXF7Pmj91H1KudbjDlrhXhZHVGKO8Flc1xtr28M0tHHsK3z6NaTh9GFFbKgx5hqgj4tf13U5DNKRptNgVCe8gguZHT-8zs5pagQ3V0RxYAgDGiTonfWpD3iAuqTgTwiDUGbhLTxHnkXTH5dvbDgs3kz3yfV74vz6-W3-urH18vl2VWtBW_HupMtEGo7AGkZa6hsiey4FtD2WIAeGik5lVZSIYaODxiblljTk0YQBpr07KR6v_fd-JjVvLWsCCNlPaTtmsK43DOGCLdqk9wa0lZFcOofENNKQRqd9kZxqhsmOJacyAZj2Q6Uas47BsAt6Wnx-jJXm_q1GbQJYwJ_YHr4E9yNWsU7xSihXMhi8HE2SPHPZPKo1i7vtgbBxCmrDhcWpgQX5of_mE8PN7NWUPp3wcZSVu881VkjRSsYlTuvxROscgazdrokzLqCHwiavUCnmHMy9mFEgtUun_fNqF0-1ZzPInv3eD0PovtAsr-VHOB9</recordid><startdate>20111109</startdate><enddate>20111109</enddate><creator>Morandi, Andrea</creator><creator>Barbetti, Valentina</creator><creator>Riverso, Maria</creator><creator>Dello Sbarba, Persio</creator><creator>Rovida, Elisabetta</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20111109</creationdate><title>The colony-stimulating factor-1 (CSF-1) receptor sustains ERK1/2 activation and proliferation in breast cancer cell lines</title><author>Morandi, Andrea ; Barbetti, Valentina ; Riverso, Maria ; Dello Sbarba, Persio ; Rovida, Elisabetta</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c658t-978a12f9aa7f3342781795c6a8b06acd477527f7266d95d00e81feb14613ac1b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Autocrine signalling</topic><topic>Benzamides</topic><topic>Binding sites</topic><topic>Biocompatibility</topic><topic>Biology</topic><topic>Biomedical materials</topic><topic>Biotechnology</topic><topic>Blotting, Western</topic><topic>Breast cancer</topic><topic>Breast carcinoma</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>c-Jun protein</topic><topic>c-Myc protein</topic><topic>Cancer</topic><topic>Cancer research</topic><topic>Cancer therapies</topic><topic>Cell activation</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Colonies</topic><topic>Colony-stimulating factor</topic><topic>Cyclin D1</topic><topic>Electrophoresis, Polyacrylamide Gel</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Extracellular signal-regulated kinase</topic><topic>Fibroblasts</topic><topic>Flow Cytometry</topic><topic>Gene expression</topic><topic>Genomes</topic><topic>Health aspects</topic><topic>Hep G2 Cells</topic><topic>Humans</topic><topic>Imatinib</topic><topic>Imatinib Mesylate</topic><topic>Immunoblotting</topic><topic>Implantation</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Ligands</topic><topic>Macrophage colony stimulating factor</topic><topic>Macrophage Colony-Stimulating Factor - metabolism</topic><topic>Macrophage Colony-Stimulating Factor - pharmacology</topic><topic>Macrophages</topic><topic>Mammary gland</topic><topic>Medical prognosis</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mitogen-Activated Protein Kinase 1 - genetics</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - genetics</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Mutation</topic><topic>Myc protein</topic><topic>NIH 3T3 Cells</topic><topic>Phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Piperazines - pharmacology</topic><topic>Prognosis</topic><topic>Pyrimidines - pharmacology</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Receptor, Macrophage Colony-Stimulating Factor - genetics</topic><topic>Receptor, Macrophage Colony-Stimulating Factor - metabolism</topic><topic>RNA, Small Interfering - genetics</topic><topic>Signal transduction</topic><topic>siRNA</topic><topic>Transcription factors</topic><topic>Transgenic animals</topic><topic>Tumor cell lines</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morandi, Andrea</creatorcontrib><creatorcontrib>Barbetti, Valentina</creatorcontrib><creatorcontrib>Riverso, Maria</creatorcontrib><creatorcontrib>Dello Sbarba, Persio</creatorcontrib><creatorcontrib>Rovida, Elisabetta</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morandi, Andrea</au><au>Barbetti, Valentina</au><au>Riverso, Maria</au><au>Dello Sbarba, Persio</au><au>Rovida, Elisabetta</au><au>Ulasov, Ilya</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The colony-stimulating factor-1 (CSF-1) receptor sustains ERK1/2 activation and proliferation in breast cancer cell lines</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2011-11-09</date><risdate>2011</risdate><volume>6</volume><issue>11</issue><spage>e27450</spage><epage>e27450</epage><pages>e27450-e27450</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Breast cancer is the second leading cause of cancer-related deaths in western countries. Colony-Stimulating Factor-1 (CSF-1) and its receptor (CSF-1R) regulate macrophage and osteoclast production, trophoblast implantation and mammary gland development. The expression of CSF-1R and/or CSF-1 strongly correlates with poor prognosis in several human epithelial tumors, including breast carcinomas. We demonstrate that CSF-1 and CSF-1R are expressed, although at different levels, in 16/17 breast cancer cell lines tested with no differences among molecular subtypes. The role of CSF-1/CSF-1R in the proliferation of breast cancer cells was then studied in MDAMB468 and SKBR3 cells belonging to different subtypes. CSF-1 administration induced ERK1/2 phosphorylation and enhanced cell proliferation in both cell lines. Furthermore, the inhibition of CSF-1/CSF-1R signaling, by CSF-1R siRNA or imatinib treatment, impaired CSF-1 induced ERK1/2 activation and cell proliferation. We also demonstrate that c-Jun, cyclin D1 and c-Myc, known for their involvement in cell proliferation, are downstream CSF-1R in breast cancer cells. The presence of a proliferative CSF-1/CSF-1R autocrine loop involving ERK1/2 was also found. The wide expression of the CSF-1/CSF-1R pair across breast cancer cell subtypes supports CSF-1/CSF-1R targeting in breast cancer therapy.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22096574</pmid><doi>10.1371/journal.pone.0027450</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2011-11, Vol.6 (11), p.e27450-e27450 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1311931894 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals Apoptosis Autocrine signalling Benzamides Binding sites Biocompatibility Biology Biomedical materials Biotechnology Blotting, Western Breast cancer Breast carcinoma Breast Neoplasms - genetics Breast Neoplasms - metabolism c-Jun protein c-Myc protein Cancer Cancer research Cancer therapies Cell activation Cell cycle Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - drug effects Colonies Colony-stimulating factor Cyclin D1 Electrophoresis, Polyacrylamide Gel Enzyme-Linked Immunosorbent Assay Extracellular signal-regulated kinase Fibroblasts Flow Cytometry Gene expression Genomes Health aspects Hep G2 Cells Humans Imatinib Imatinib Mesylate Immunoblotting Implantation Kinases Laboratories Ligands Macrophage colony stimulating factor Macrophage Colony-Stimulating Factor - metabolism Macrophage Colony-Stimulating Factor - pharmacology Macrophages Mammary gland Medical prognosis Medical research Medicine Metabolism Mice Mitogen-Activated Protein Kinase 1 - genetics Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - genetics Mitogen-Activated Protein Kinase 3 - metabolism Mutation Myc protein NIH 3T3 Cells Phosphorylation Phosphorylation - drug effects Piperazines - pharmacology Prognosis Pyrimidines - pharmacology Real-Time Polymerase Chain Reaction Receptor, Macrophage Colony-Stimulating Factor - genetics Receptor, Macrophage Colony-Stimulating Factor - metabolism RNA, Small Interfering - genetics Signal transduction siRNA Transcription factors Transgenic animals Tumor cell lines Tumorigenesis Tumors |
| title | The colony-stimulating factor-1 (CSF-1) receptor sustains ERK1/2 activation and proliferation in breast cancer cell lines |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-08T01%3A12%3A43IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20colony-stimulating%20factor-1%20(CSF-1)%20receptor%20sustains%20ERK1/2%20activation%20and%20proliferation%20in%20breast%20cancer%20cell%20lines&rft.jtitle=PloS%20one&rft.au=Morandi,%20Andrea&rft.date=2011-11-09&rft.volume=6&rft.issue=11&rft.spage=e27450&rft.epage=e27450&rft.pages=e27450-e27450&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0027450&rft_dat=%3Cgale_plos_%3EA476863270%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1311931894&rft_id=info:pmid/22096574&rft_galeid=A476863270&rft_doaj_id=oai_doaj_org_article_52c43650751740078d22c5593aa5f1b2&rfr_iscdi=true |