Induction of Signalling in Non-Erythroid Cells by Pharmacological Levels of Erythropoietin
Erythropoiesis is maintained by the hormone erythropoietin (Epo) binding to its cognate receptor (EpoR) on erythroid progenitor cells. The Epo-EpoR interaction initiates a signal transduction process that regulates the survival, growth and differentiation of these cells. Originally perceived as high...
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| Veröffentlicht in: | Neuro-degenerative diseases 2006-01, Vol.3 (1-2), p.94-100 |
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| creator | Dunlop, E.A. Percy, M.J. Boland, M.P. Maxwell, A.P. Lappin, T.R. |
| description | Erythropoiesis is maintained by the hormone erythropoietin (Epo) binding to its cognate receptor (EpoR) on erythroid progenitor cells. The Epo-EpoR interaction initiates a signal transduction process that regulates the survival, growth and differentiation of these cells. Originally perceived as highly lineage-restricted, Epo is now recognised to have pleiotropic effects extending beyond the maintenance of red cell mass. Functional interactions between Epo and EpoR have been demonstrated in numerous cells and tissues. EpoR expression on neoplastic cells leads to concern that recombinant human erythropoietin, used to treat anaemia in cancer patients, may augment tumour growth. Here we demonstrate that EPO, at pharmacological concentrations, can activate three major signalling cascades, viz. the Jak2/STAT5, Ras/ERK and PI3K/Akt pathways in non-small cell lung carcinoma (NSCLC) cell lines. EpoR synthesis is normally under the control of GATA-1, but NSCLC cells exhibit decreased GATA-1 levels compared to GATA-2, -3 and -6, suggesting that GATA-1 is not essential for EpoR production. The increased Epo-induced signalling was not associated with a growth advantage for the NSCLC cells. |
| doi_str_mv | 10.1159/000092099 |
| format | Article |
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The Epo-EpoR interaction initiates a signal transduction process that regulates the survival, growth and differentiation of these cells. Originally perceived as highly lineage-restricted, Epo is now recognised to have pleiotropic effects extending beyond the maintenance of red cell mass. Functional interactions between Epo and EpoR have been demonstrated in numerous cells and tissues. EpoR expression on neoplastic cells leads to concern that recombinant human erythropoietin, used to treat anaemia in cancer patients, may augment tumour growth. Here we demonstrate that EPO, at pharmacological concentrations, can activate three major signalling cascades, viz. the Jak2/STAT5, Ras/ERK and PI3K/Akt pathways in non-small cell lung carcinoma (NSCLC) cell lines. EpoR synthesis is normally under the control of GATA-1, but NSCLC cells exhibit decreased GATA-1 levels compared to GATA-2, -3 and -6, suggesting that GATA-1 is not essential for EpoR production. The increased Epo-induced signalling was not associated with a growth advantage for the NSCLC cells.</description><identifier>ISSN: 1660-2854</identifier><identifier>ISBN: 9783805581394</identifier><identifier>ISBN: 3805581394</identifier><identifier>EISSN: 1660-2862</identifier><identifier>EISBN: 9783318013658</identifier><identifier>EISBN: 331801365X</identifier><identifier>DOI: 10.1159/000092099</identifier><identifier>PMID: 16909043</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Carcinoma, Non-Small-Cell Lung ; Cell Division - drug effects ; Cell Division - physiology ; Cell Line, Tumor ; Erythroid Cells - cytology ; Erythroid Cells - metabolism ; Erythropoietin - metabolism ; Erythropoietin - pharmacology ; GATA1 Transcription Factor - genetics ; GATA2 Transcription Factor - genetics ; GATA3 Transcription Factor - genetics ; GATA4 Transcription Factor - genetics ; GATA5 Transcription Factor - genetics ; GATA6 Transcription Factor - genetics ; Gene Expression - physiology ; Humans ; Lung Neoplasms ; Receptors, Erythropoietin - genetics ; Receptors, Erythropoietin - metabolism ; Recombinant Proteins ; RNA, Messenger - analysis ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Signaling and Stem Cells</subject><ispartof>Neuro-degenerative diseases, 2006-01, Vol.3 (1-2), p.94-100</ispartof><rights>2006 S. Karger AG, Basel</rights><rights>Copyright (c) 2006 S. 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The increased Epo-induced signalling was not associated with a growth advantage for the NSCLC cells.</description><subject>Carcinoma, Non-Small-Cell Lung</subject><subject>Cell Division - drug effects</subject><subject>Cell Division - physiology</subject><subject>Cell Line, Tumor</subject><subject>Erythroid Cells - cytology</subject><subject>Erythroid Cells - metabolism</subject><subject>Erythropoietin - metabolism</subject><subject>Erythropoietin - pharmacology</subject><subject>GATA1 Transcription Factor - genetics</subject><subject>GATA2 Transcription Factor - genetics</subject><subject>GATA3 Transcription Factor - genetics</subject><subject>GATA4 Transcription Factor - genetics</subject><subject>GATA5 Transcription Factor - genetics</subject><subject>GATA6 Transcription Factor - genetics</subject><subject>Gene Expression - physiology</subject><subject>Humans</subject><subject>Lung Neoplasms</subject><subject>Receptors, Erythropoietin - genetics</subject><subject>Receptors, Erythropoietin - metabolism</subject><subject>Recombinant Proteins</subject><subject>RNA, Messenger - analysis</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Signaling and Stem Cells</subject><issn>1660-2854</issn><issn>1660-2862</issn><isbn>9783805581394</isbn><isbn>3805581394</isbn><isbn>9783318013658</isbn><isbn>331801365X</isbn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</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>eNpF0M9LwzAUB_D4CzfnDp4FKXjyUH1pmiY5ypg6GCq4k5eSNkmX2TUzbYX991ZaZi7v8P28B_kidIXhHmMqHqB7IgIhjtBUME4I5oBJQvkxGuMkgTDiSXTSZxwo5ZiI-PSQ0XiELup6AxAJJvA5GuFEgICYjNHnolJt3lhXBc4EH7aoZFnaqghsFby6Kpz7fbP2zqpgpsuyDrJ98L6WfitzV7rC5rIMlvpHd0m3PuCds7qx1SU6M7Ks9XSYE7R6mq9mL-Hy7Xkxe1yGOQFoQsmZNkIC59pQTRRVjDGQTHBqwGCtJEQcx9owarARIJXMpMpIHimWSCATdNuf3Xn33eq6STeu9d036hRDIkgiMCOduutV7l1de23Snbdb6fcdSv9KTg8ld_ZmuNhmW63-5dBaB6578CV9of0B9Ou_PQV7Og</recordid><startdate>20060101</startdate><enddate>20060101</enddate><creator>Dunlop, E.A.</creator><creator>Percy, M.J.</creator><creator>Boland, M.P.</creator><creator>Maxwell, A.P.</creator><creator>Lappin, T.R.</creator><general>S. 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drug effects</topic><topic>Cell Division - physiology</topic><topic>Cell Line, Tumor</topic><topic>Erythroid Cells - cytology</topic><topic>Erythroid Cells - metabolism</topic><topic>Erythropoietin - metabolism</topic><topic>Erythropoietin - pharmacology</topic><topic>GATA1 Transcription Factor - genetics</topic><topic>GATA2 Transcription Factor - genetics</topic><topic>GATA3 Transcription Factor - genetics</topic><topic>GATA4 Transcription Factor - genetics</topic><topic>GATA5 Transcription Factor - genetics</topic><topic>GATA6 Transcription Factor - genetics</topic><topic>Gene Expression - physiology</topic><topic>Humans</topic><topic>Lung Neoplasms</topic><topic>Receptors, Erythropoietin - genetics</topic><topic>Receptors, Erythropoietin - metabolism</topic><topic>Recombinant Proteins</topic><topic>RNA, Messenger - analysis</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Signaling and Stem Cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dunlop, E.A.</creatorcontrib><creatorcontrib>Percy, M.J.</creatorcontrib><creatorcontrib>Boland, M.P.</creatorcontrib><creatorcontrib>Maxwell, A.P.</creatorcontrib><creatorcontrib>Lappin, T.R.</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>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech 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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Neuro-degenerative diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dunlop, E.A.</au><au>Percy, M.J.</au><au>Boland, M.P.</au><au>Maxwell, A.P.</au><au>Lappin, T.R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction of Signalling in Non-Erythroid Cells by Pharmacological Levels of Erythropoietin</atitle><jtitle>Neuro-degenerative diseases</jtitle><addtitle>Neurodegener Dis</addtitle><date>2006-01-01</date><risdate>2006</risdate><volume>3</volume><issue>1-2</issue><spage>94</spage><epage>100</epage><pages>94-100</pages><issn>1660-2854</issn><eissn>1660-2862</eissn><isbn>9783805581394</isbn><isbn>3805581394</isbn><eisbn>9783318013658</eisbn><eisbn>331801365X</eisbn><abstract>Erythropoiesis is maintained by the hormone erythropoietin (Epo) binding to its cognate receptor (EpoR) on erythroid progenitor cells. The Epo-EpoR interaction initiates a signal transduction process that regulates the survival, growth and differentiation of these cells. Originally perceived as highly lineage-restricted, Epo is now recognised to have pleiotropic effects extending beyond the maintenance of red cell mass. Functional interactions between Epo and EpoR have been demonstrated in numerous cells and tissues. EpoR expression on neoplastic cells leads to concern that recombinant human erythropoietin, used to treat anaemia in cancer patients, may augment tumour growth. Here we demonstrate that EPO, at pharmacological concentrations, can activate three major signalling cascades, viz. the Jak2/STAT5, Ras/ERK and PI3K/Akt pathways in non-small cell lung carcinoma (NSCLC) cell lines. EpoR synthesis is normally under the control of GATA-1, but NSCLC cells exhibit decreased GATA-1 levels compared to GATA-2, -3 and -6, suggesting that GATA-1 is not essential for EpoR production. The increased Epo-induced signalling was not associated with a growth advantage for the NSCLC cells.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>16909043</pmid><doi>10.1159/000092099</doi><tpages>7</tpages></addata></record> |
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| ispartof | Neuro-degenerative diseases, 2006-01, Vol.3 (1-2), p.94-100 |
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| language | eng |
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| source | MEDLINE; Karger Journals |
| subjects | Carcinoma, Non-Small-Cell Lung Cell Division - drug effects Cell Division - physiology Cell Line, Tumor Erythroid Cells - cytology Erythroid Cells - metabolism Erythropoietin - metabolism Erythropoietin - pharmacology GATA1 Transcription Factor - genetics GATA2 Transcription Factor - genetics GATA3 Transcription Factor - genetics GATA4 Transcription Factor - genetics GATA5 Transcription Factor - genetics GATA6 Transcription Factor - genetics Gene Expression - physiology Humans Lung Neoplasms Receptors, Erythropoietin - genetics Receptors, Erythropoietin - metabolism Recombinant Proteins RNA, Messenger - analysis Signal Transduction - drug effects Signal Transduction - physiology Signaling and Stem Cells |
| title | Induction of Signalling in Non-Erythroid Cells by Pharmacological Levels of Erythropoietin |
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