A crosstalk between the Wnt and the adhesion-dependent signaling pathways governs the chemosensitivity of acute myeloid leukemia
Relapses following chemotherapy are a major hindrance to patients' survival in acute myeloid leukemia (AML). To investigate the role of the hematopoietic niche in the chemoresistance of leukemic cells, we examined two pathways: one mediated by adhesion molecules/integrins, and the other by solu...
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| Veröffentlicht in: | Oncogene 2006-05, Vol.25 (22), p.3113-3122 |
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| creator | DE TONI, F RACAUD-SULTAN, C MANENTI, S YSEBAERT, L CHICANNE, G MANSAT-DE MAS, V CARIVEN, C MESANGE, F SALLES, J.-P DEMUR, C ALLOUCHE, M PAYRASTRE, B |
| description | Relapses following chemotherapy are a major hindrance to patients' survival in acute myeloid leukemia (AML). To investigate the role of the hematopoietic niche in the chemoresistance of leukemic cells, we examined two pathways: one mediated by adhesion molecules/integrins, and the other by soluble factors of the morphogen Wnt pathway. In our study, both the adhesion of leukemic blasts to fibronectin and the addition of Wnt antagonists induced, independently, resistance of AML cells to daunorubicin in a cell survival assay. Using pharmacological inhibitors and siRNA, we showed that both resistance pathways required the activity of the glycogen synthase kinase 3beta (GSK3beta). Moreover, the AML cell protection downstream of GSK3beta was mediated by NF-kappaB. A link between the adhesion and the Wnt pathway was found, as adhesion of U937 on human osteoblasts, a component of the hematopoietic niche, triggered the secretion of the Wnt antagonist sFRP-1 and supported resistance to daunorubicin. The osteoblast-conditioned medium could also confer chemoresistance to U937 cells cultured in suspension, and this cell protective effect was abrogated after depletion of sFRP-1. In the context of this potential double in vivo resistance, modulators of the common signal GSK3beta and of its target NF-kappaB could represent important novel therapeutic tools. |
| doi_str_mv | 10.1038/sj.onc.1209346 |
| format | Article |
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To investigate the role of the hematopoietic niche in the chemoresistance of leukemic cells, we examined two pathways: one mediated by adhesion molecules/integrins, and the other by soluble factors of the morphogen Wnt pathway. In our study, both the adhesion of leukemic blasts to fibronectin and the addition of Wnt antagonists induced, independently, resistance of AML cells to daunorubicin in a cell survival assay. Using pharmacological inhibitors and siRNA, we showed that both resistance pathways required the activity of the glycogen synthase kinase 3beta (GSK3beta). Moreover, the AML cell protection downstream of GSK3beta was mediated by NF-kappaB. A link between the adhesion and the Wnt pathway was found, as adhesion of U937 on human osteoblasts, a component of the hematopoietic niche, triggered the secretion of the Wnt antagonist sFRP-1 and supported resistance to daunorubicin. The osteoblast-conditioned medium could also confer chemoresistance to U937 cells cultured in suspension, and this cell protective effect was abrogated after depletion of sFRP-1. In the context of this potential double in vivo resistance, modulators of the common signal GSK3beta and of its target NF-kappaB could represent important novel therapeutic tools.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1209346</identifier><identifier>PMID: 16407823</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>Acute myeloid leukemia ; Antagonists ; Antibiotics, Antineoplastic - pharmacology ; Biological and medical sciences ; Blast Crisis ; Cell adhesion & migration ; Cell Adhesion - drug effects ; Cell adhesion molecules ; Cell physiology ; Cell survival ; Cell Survival - drug effects ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cells, Cultured ; Cellular biology ; Chemoresistance ; Chemotherapy ; Culture Media, Conditioned - pharmacology ; Daunorubicin ; Daunorubicin - pharmacology ; Drug Resistance, Neoplasm ; Fibronectin ; Fibronectins - metabolism ; Frizzled-related protein 1 ; Fundamental and applied biological sciences. Psychology ; Glycogen ; Glycogen synthase kinase 3 ; Glycogen Synthase Kinase 3 - metabolism ; Glycogen Synthase Kinase 3 beta ; Hematologic and hematopoietic diseases ; Humans ; Inhibitor drugs ; Integrins ; Intercellular Signaling Peptides and Proteins - metabolism ; Leukemia ; Leukemia, Myeloid, Acute - drug therapy ; Leukemia, Myeloid, Acute - metabolism ; Leukemia, Myeloid, Acute - pathology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Medical sciences ; Membrane Proteins - metabolism ; Molecular and cellular biology ; NF-kappa B - genetics ; NF-kappa B - metabolism ; NF-κB protein ; Oncology ; Osteoblasts ; Osteoblasts - cytology ; Osteoblasts - metabolism ; RNA, Small Interfering - pharmacology ; Signal Transduction ; siRNA ; U937 Cells - metabolism ; Wnt protein ; Wnt Proteins - metabolism</subject><ispartof>Oncogene, 2006-05, Vol.25 (22), p.3113-3122</ispartof><rights>2006 INIST-CNRS</rights><rights>COPYRIGHT 2006 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group May 25, 2006</rights><rights>Nature Publishing Group 2006.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c569t-a2c5a146f7477c4766ed4a6e65cee8cd5c2ebfaf777e479307a89a0e1cbde8fb3</citedby><cites>FETCH-LOGICAL-c569t-a2c5a146f7477c4766ed4a6e65cee8cd5c2ebfaf777e479307a89a0e1cbde8fb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,2731,27933,27934</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17795009$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16407823$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DE TONI, F</creatorcontrib><creatorcontrib>RACAUD-SULTAN, C</creatorcontrib><creatorcontrib>MANENTI, S</creatorcontrib><creatorcontrib>YSEBAERT, L</creatorcontrib><creatorcontrib>CHICANNE, G</creatorcontrib><creatorcontrib>MANSAT-DE MAS, V</creatorcontrib><creatorcontrib>CARIVEN, C</creatorcontrib><creatorcontrib>MESANGE, F</creatorcontrib><creatorcontrib>SALLES, J.-P</creatorcontrib><creatorcontrib>DEMUR, C</creatorcontrib><creatorcontrib>ALLOUCHE, M</creatorcontrib><creatorcontrib>PAYRASTRE, B</creatorcontrib><title>A crosstalk between the Wnt and the adhesion-dependent signaling pathways governs the chemosensitivity of acute myeloid leukemia</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>Relapses following chemotherapy are a major hindrance to patients' survival in acute myeloid leukemia (AML). To investigate the role of the hematopoietic niche in the chemoresistance of leukemic cells, we examined two pathways: one mediated by adhesion molecules/integrins, and the other by soluble factors of the morphogen Wnt pathway. In our study, both the adhesion of leukemic blasts to fibronectin and the addition of Wnt antagonists induced, independently, resistance of AML cells to daunorubicin in a cell survival assay. Using pharmacological inhibitors and siRNA, we showed that both resistance pathways required the activity of the glycogen synthase kinase 3beta (GSK3beta). Moreover, the AML cell protection downstream of GSK3beta was mediated by NF-kappaB. A link between the adhesion and the Wnt pathway was found, as adhesion of U937 on human osteoblasts, a component of the hematopoietic niche, triggered the secretion of the Wnt antagonist sFRP-1 and supported resistance to daunorubicin. The osteoblast-conditioned medium could also confer chemoresistance to U937 cells cultured in suspension, and this cell protective effect was abrogated after depletion of sFRP-1. In the context of this potential double in vivo resistance, modulators of the common signal GSK3beta and of its target NF-kappaB could represent important novel therapeutic tools.</description><subject>Acute myeloid leukemia</subject><subject>Antagonists</subject><subject>Antibiotics, Antineoplastic - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blast Crisis</subject><subject>Cell adhesion & migration</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell adhesion molecules</subject><subject>Cell physiology</subject><subject>Cell survival</subject><subject>Cell Survival - drug effects</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cells, Cultured</subject><subject>Cellular biology</subject><subject>Chemoresistance</subject><subject>Chemotherapy</subject><subject>Culture Media, Conditioned - pharmacology</subject><subject>Daunorubicin</subject><subject>Daunorubicin - pharmacology</subject><subject>Drug Resistance, Neoplasm</subject><subject>Fibronectin</subject><subject>Fibronectins - metabolism</subject><subject>Frizzled-related protein 1</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glycogen</subject><subject>Glycogen synthase kinase 3</subject><subject>Glycogen Synthase Kinase 3 - metabolism</subject><subject>Glycogen Synthase Kinase 3 beta</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Inhibitor drugs</subject><subject>Integrins</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Leukemia</subject><subject>Leukemia, Myeloid, Acute - drug therapy</subject><subject>Leukemia, Myeloid, Acute - metabolism</subject><subject>Leukemia, Myeloid, Acute - pathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>Membrane Proteins - metabolism</subject><subject>Molecular and cellular biology</subject><subject>NF-kappa B - genetics</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Oncology</subject><subject>Osteoblasts</subject><subject>Osteoblasts - cytology</subject><subject>Osteoblasts - metabolism</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>Signal Transduction</subject><subject>siRNA</subject><subject>U937 Cells - metabolism</subject><subject>Wnt protein</subject><subject>Wnt Proteins - metabolism</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFks1v1DAQxSMEotvClRvIooJbFjt27Pi4qviSKnEBcYwmzmTX28ReYqfV3vjT8W4jLUJFlQ-27N-8Nx69LHvF6JJRXn0I26V3ZskKqrmQT7IFE0rmZanF02xBdUlzXfDiLDsPYUspVZoWz7MzJgVVVcEX2e8VMaMPIUJ_QxqMd4iOxA2Sny4ScO3xDO0Gg_Uub3GHrsX0FOzaQW_dmuwgbu5gH8ja3-LowrHCbHDwAV2w0d7auCe-I2CmiGTYY-9tS3qcbnCw8CJ71kEf8OW8X2Q_Pn38fvUlv_72-evV6jo3pdQxh8KUwITslFDKpD9KbAVIlKVBrExbmgKbDjqlFAqlOVVQaaDITNNi1TX8Int_r7sb_a8JQ6wHGwz2PTj0U6hlRRlLo3oULBjnlHP9KMi0KiquD4qX_4BbP41pfElMCsbLUlQiUW__SxWKC12Jv6TW0GNtXefjCObgW69YpWkpOT10tnyASqtNEzfeYWfT_UMFxyyM2NW70Q4w7mtG60PO6rCtU87qOWep4M3c7NQM2J7wOVgJeDcDEAz03QjO2HDilErZPDq_vuccxGnEEzAb_QF2y-Wf</recordid><startdate>20060525</startdate><enddate>20060525</enddate><creator>DE TONI, F</creator><creator>RACAUD-SULTAN, C</creator><creator>MANENTI, S</creator><creator>YSEBAERT, L</creator><creator>CHICANNE, G</creator><creator>MANSAT-DE MAS, V</creator><creator>CARIVEN, C</creator><creator>MESANGE, F</creator><creator>SALLES, J.-P</creator><creator>DEMUR, C</creator><creator>ALLOUCHE, M</creator><creator>PAYRASTRE, B</creator><general>Nature Publishing</general><general>Nature Publishing Group</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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7T5</scope><scope>7X8</scope></search><sort><creationdate>20060525</creationdate><title>A crosstalk between the Wnt and the adhesion-dependent signaling pathways governs the chemosensitivity of acute myeloid leukemia</title><author>DE TONI, F ; RACAUD-SULTAN, C ; MANENTI, S ; YSEBAERT, L ; CHICANNE, G ; MANSAT-DE MAS, V ; CARIVEN, C ; MESANGE, F ; SALLES, J.-P ; DEMUR, C ; ALLOUCHE, M ; PAYRASTRE, B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c569t-a2c5a146f7477c4766ed4a6e65cee8cd5c2ebfaf777e479307a89a0e1cbde8fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Acute myeloid leukemia</topic><topic>Antagonists</topic><topic>Antibiotics, Antineoplastic - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blast Crisis</topic><topic>Cell adhesion & migration</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell adhesion molecules</topic><topic>Cell physiology</topic><topic>Cell survival</topic><topic>Cell Survival - drug effects</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Cells, Cultured</topic><topic>Cellular biology</topic><topic>Chemoresistance</topic><topic>Chemotherapy</topic><topic>Culture Media, Conditioned - pharmacology</topic><topic>Daunorubicin</topic><topic>Daunorubicin - pharmacology</topic><topic>Drug Resistance, Neoplasm</topic><topic>Fibronectin</topic><topic>Fibronectins - metabolism</topic><topic>Frizzled-related protein 1</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glycogen</topic><topic>Glycogen synthase kinase 3</topic><topic>Glycogen Synthase Kinase 3 - metabolism</topic><topic>Glycogen Synthase Kinase 3 beta</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Inhibitor drugs</topic><topic>Integrins</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Leukemia</topic><topic>Leukemia, Myeloid, Acute - drug therapy</topic><topic>Leukemia, Myeloid, Acute - metabolism</topic><topic>Leukemia, Myeloid, Acute - pathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>Membrane Proteins - metabolism</topic><topic>Molecular and cellular biology</topic><topic>NF-kappa B - genetics</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Oncology</topic><topic>Osteoblasts</topic><topic>Osteoblasts - cytology</topic><topic>Osteoblasts - metabolism</topic><topic>RNA, Small Interfering - pharmacology</topic><topic>Signal Transduction</topic><topic>siRNA</topic><topic>U937 Cells - metabolism</topic><topic>Wnt protein</topic><topic>Wnt Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DE TONI, F</creatorcontrib><creatorcontrib>RACAUD-SULTAN, C</creatorcontrib><creatorcontrib>MANENTI, S</creatorcontrib><creatorcontrib>YSEBAERT, L</creatorcontrib><creatorcontrib>CHICANNE, G</creatorcontrib><creatorcontrib>MANSAT-DE MAS, V</creatorcontrib><creatorcontrib>CARIVEN, C</creatorcontrib><creatorcontrib>MESANGE, F</creatorcontrib><creatorcontrib>SALLES, J.-P</creatorcontrib><creatorcontrib>DEMUR, C</creatorcontrib><creatorcontrib>ALLOUCHE, M</creatorcontrib><creatorcontrib>PAYRASTRE, B</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>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</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 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>Research Library (Alumni Edition)</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>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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 Central Basic</collection><collection>Genetics Abstracts</collection><collection>Immunology Abstracts</collection><collection>MEDLINE - 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The osteoblast-conditioned medium could also confer chemoresistance to U937 cells cultured in suspension, and this cell protective effect was abrogated after depletion of sFRP-1. In the context of this potential double in vivo resistance, modulators of the common signal GSK3beta and of its target NF-kappaB could represent important novel therapeutic tools.</abstract><cop>Basingstoke</cop><pub>Nature Publishing</pub><pmid>16407823</pmid><doi>10.1038/sj.onc.1209346</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncogene, 2006-05, Vol.25 (22), p.3113-3122 |
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| language | eng |
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| source | MEDLINE; Nature; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Acute myeloid leukemia Antagonists Antibiotics, Antineoplastic - pharmacology Biological and medical sciences Blast Crisis Cell adhesion & migration Cell Adhesion - drug effects Cell adhesion molecules Cell physiology Cell survival Cell Survival - drug effects Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cells, Cultured Cellular biology Chemoresistance Chemotherapy Culture Media, Conditioned - pharmacology Daunorubicin Daunorubicin - pharmacology Drug Resistance, Neoplasm Fibronectin Fibronectins - metabolism Frizzled-related protein 1 Fundamental and applied biological sciences. Psychology Glycogen Glycogen synthase kinase 3 Glycogen Synthase Kinase 3 - metabolism Glycogen Synthase Kinase 3 beta Hematologic and hematopoietic diseases Humans Inhibitor drugs Integrins Intercellular Signaling Peptides and Proteins - metabolism Leukemia Leukemia, Myeloid, Acute - drug therapy Leukemia, Myeloid, Acute - metabolism Leukemia, Myeloid, Acute - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Membrane Proteins - metabolism Molecular and cellular biology NF-kappa B - genetics NF-kappa B - metabolism NF-κB protein Oncology Osteoblasts Osteoblasts - cytology Osteoblasts - metabolism RNA, Small Interfering - pharmacology Signal Transduction siRNA U937 Cells - metabolism Wnt protein Wnt Proteins - metabolism |
| title | A crosstalk between the Wnt and the adhesion-dependent signaling pathways governs the chemosensitivity of acute myeloid leukemia |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-03T11%3A09%3A10IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=A%20crosstalk%20between%20the%20Wnt%20and%20the%20adhesion-dependent%20signaling%20pathways%20governs%20the%20chemosensitivity%20of%20acute%20myeloid%20leukemia&rft.jtitle=Oncogene&rft.au=DE%20TONI,%20F&rft.date=2006-05-25&rft.volume=25&rft.issue=22&rft.spage=3113&rft.epage=3122&rft.pages=3113-3122&rft.issn=0950-9232&rft.eissn=1476-5594&rft.coden=ONCNES&rft_id=info:doi/10.1038/sj.onc.1209346&rft_dat=%3Cgale_proqu%3EA189056309%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=227349842&rft_id=info:pmid/16407823&rft_galeid=A189056309&rfr_iscdi=true |