Hydroquinone modulates the GM-CSF signaling pathway in TF-1 cells
Human leukemogens, including alkylating chemotherapeutic agents and benzene, enhance granulocyte–macrophage colony-stimulating factor (GM-CSF)-dependent proliferation of human CD34+ bone marrow (BM) cells. The extracellular signal-regulated kinase (ERK) pathway plays an important role in GM-CSF-depe...
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| Veröffentlicht in: | Leukemia 2004-07, Vol.18 (7), p.1296-1304 |
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| creator | Zheng, J H Pyatt, D W Gross, S A Le, A T Kerzic, P J Irons, R D |
| description | Human leukemogens, including alkylating chemotherapeutic agents and benzene, enhance granulocyte–macrophage colony-stimulating factor (GM-CSF)-dependent proliferation of human CD34+ bone marrow (BM) cells. The extracellular signal-regulated kinase (ERK) pathway plays an important role in GM-CSF-dependent proliferation and also has been implicated in the pathogenesis of acute myelogenous leukemia. Therefore, we investigated the effects of the benzene metabolite, hydroquinone (HQ), on alterations in the GM-CSF signaling pathway in TF-1 erythroleukemia cells and human CD34+ BM cells. HQ treatment in TF-1 cells results in a strong proliferative response that is dependent on ERK activation and GM-CSF production. HQ also induces ERK-dependent AP-1 activation with concomitant increased transcriptional activity of AP-1 reporter gene. However, the kinetics of ERK activation are different between rhGM-CSF and HQ in TF-1 cells: rhGM-CSF results in immediate activation of ERK, whereas HQ activation of ERK is delayed. Further, HQ and rhGM-CSF together produce an immediate increase in ERK phosphorylation, which is sustained for over 48 h. HQ also stimulates colony formation, AP-1 DNA binding and GM-CSF production in human CD34+ BM cells. These results suggest that HQ stimulates proliferation via activation of ERK/AP-1 and is at least partially mediated via the production of GM-CSF. |
| doi_str_mv | 10.1038/sj.leu.2403389 |
| format | Article |
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The extracellular signal-regulated kinase (ERK) pathway plays an important role in GM-CSF-dependent proliferation and also has been implicated in the pathogenesis of acute myelogenous leukemia. Therefore, we investigated the effects of the benzene metabolite, hydroquinone (HQ), on alterations in the GM-CSF signaling pathway in TF-1 erythroleukemia cells and human CD34+ BM cells. HQ treatment in TF-1 cells results in a strong proliferative response that is dependent on ERK activation and GM-CSF production. HQ also induces ERK-dependent AP-1 activation with concomitant increased transcriptional activity of AP-1 reporter gene. However, the kinetics of ERK activation are different between rhGM-CSF and HQ in TF-1 cells: rhGM-CSF results in immediate activation of ERK, whereas HQ activation of ERK is delayed. Further, HQ and rhGM-CSF together produce an immediate increase in ERK phosphorylation, which is sustained for over 48 h. HQ also stimulates colony formation, AP-1 DNA binding and GM-CSF production in human CD34+ BM cells. These results suggest that HQ stimulates proliferation via activation of ERK/AP-1 and is at least partially mediated via the production of GM-CSF.</description><identifier>ISSN: 0887-6924</identifier><identifier>EISSN: 1476-5551</identifier><identifier>DOI: 10.1038/sj.leu.2403389</identifier><identifier>PMID: 15129224</identifier><identifier>CODEN: LEUKED</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Acute myeloid leukemia ; Alkylation ; Antigens, CD34 ; Benzene ; Biological and medical sciences ; Bone marrow ; Bone Marrow Cells - cytology ; Bone Marrow Cells - drug effects ; Cancer Research ; Carcinogens - pharmacology ; CD34 antigen ; Cell division ; Cell Division - drug effects ; Cell Line, Tumor ; Cell proliferation ; Chemotherapy ; Colonies ; Colony-stimulating factor ; Critical Care Medicine ; Cytokines ; Deoxyribonucleic acid ; DNA ; Erythroleukemia ; Extracellular signal-regulated kinase ; Granulocyte-macrophage colony-stimulating factor ; Granulocyte-Macrophage Colony-Stimulating Factor - biosynthesis ; Granulocyte-Macrophage Colony-Stimulating Factor - metabolism ; Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology ; Granulocytes ; Health sciences ; Hematologic and hematopoietic diseases ; Hematology ; Humans ; Hydrocarbons ; Hydroquinone ; Hydroquinones - pharmacology ; Intensive ; Internal Medicine ; Kinases ; Kinetics ; Leukemia ; Leukemia, Erythroblastic, Acute - pathology ; Leukemia, Myeloid, Acute - chemically induced ; Medical sciences ; Medicine ; Medicine & Public Health ; Metabolic pathways ; Metabolites ; Mitogen-Activated Protein Kinases - metabolism ; Oncology ; original-manuscript ; Pathogenesis ; Phosphorylation ; Recombinant Proteins ; Reporter gene ; Signal transduction ; Signal Transduction - drug effects ; Signaling ; Transcription activation ; Transcription Factor AP-1 - metabolism ; Transcription factors</subject><ispartof>Leukemia, 2004-07, Vol.18 (7), p.1296-1304</ispartof><rights>Springer Nature Limited 2004</rights><rights>2004 INIST-CNRS</rights><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jul 2004</rights><rights>Nature Publishing Group 2004.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c618t-7565c7d6eaec24fdda61b17e41320a2170baf16a48bcb5509ffe3cfc7e7b865a3</citedby><cites>FETCH-LOGICAL-c618t-7565c7d6eaec24fdda61b17e41320a2170baf16a48bcb5509ffe3cfc7e7b865a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.leu.2403389$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.leu.2403389$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15895755$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15129224$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zheng, J H</creatorcontrib><creatorcontrib>Pyatt, D W</creatorcontrib><creatorcontrib>Gross, S A</creatorcontrib><creatorcontrib>Le, A T</creatorcontrib><creatorcontrib>Kerzic, P J</creatorcontrib><creatorcontrib>Irons, R D</creatorcontrib><title>Hydroquinone modulates the GM-CSF signaling pathway in TF-1 cells</title><title>Leukemia</title><addtitle>Leukemia</addtitle><addtitle>Leukemia</addtitle><description>Human leukemogens, including alkylating chemotherapeutic agents and benzene, enhance granulocyte–macrophage colony-stimulating factor (GM-CSF)-dependent proliferation of human CD34+ bone marrow (BM) cells. The extracellular signal-regulated kinase (ERK) pathway plays an important role in GM-CSF-dependent proliferation and also has been implicated in the pathogenesis of acute myelogenous leukemia. Therefore, we investigated the effects of the benzene metabolite, hydroquinone (HQ), on alterations in the GM-CSF signaling pathway in TF-1 erythroleukemia cells and human CD34+ BM cells. HQ treatment in TF-1 cells results in a strong proliferative response that is dependent on ERK activation and GM-CSF production. HQ also induces ERK-dependent AP-1 activation with concomitant increased transcriptional activity of AP-1 reporter gene. However, the kinetics of ERK activation are different between rhGM-CSF and HQ in TF-1 cells: rhGM-CSF results in immediate activation of ERK, whereas HQ activation of ERK is delayed. Further, HQ and rhGM-CSF together produce an immediate increase in ERK phosphorylation, which is sustained for over 48 h. HQ also stimulates colony formation, AP-1 DNA binding and GM-CSF production in human CD34+ BM cells. These results suggest that HQ stimulates proliferation via activation of ERK/AP-1 and is at least partially mediated via the production of GM-CSF.</description><subject>Acute myeloid leukemia</subject><subject>Alkylation</subject><subject>Antigens, CD34</subject><subject>Benzene</subject><subject>Biological and medical sciences</subject><subject>Bone marrow</subject><subject>Bone Marrow Cells - cytology</subject><subject>Bone Marrow Cells - drug effects</subject><subject>Cancer Research</subject><subject>Carcinogens - pharmacology</subject><subject>CD34 antigen</subject><subject>Cell division</subject><subject>Cell Division - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Chemotherapy</subject><subject>Colonies</subject><subject>Colony-stimulating factor</subject><subject>Critical Care Medicine</subject><subject>Cytokines</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Erythroleukemia</subject><subject>Extracellular signal-regulated kinase</subject><subject>Granulocyte-macrophage colony-stimulating factor</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - biosynthesis</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - metabolism</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology</subject><subject>Granulocytes</subject><subject>Health sciences</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hematology</subject><subject>Humans</subject><subject>Hydrocarbons</subject><subject>Hydroquinone</subject><subject>Hydroquinones - pharmacology</subject><subject>Intensive</subject><subject>Internal Medicine</subject><subject>Kinases</subject><subject>Kinetics</subject><subject>Leukemia</subject><subject>Leukemia, Erythroblastic, Acute - pathology</subject><subject>Leukemia, Myeloid, Acute - chemically induced</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic pathways</subject><subject>Metabolites</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Oncology</subject><subject>original-manuscript</subject><subject>Pathogenesis</subject><subject>Phosphorylation</subject><subject>Recombinant Proteins</subject><subject>Reporter gene</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Transcription activation</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Transcription 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modulates the GM-CSF signaling pathway in TF-1 cells</title><author>Zheng, J H ; Pyatt, D W ; Gross, S A ; Le, A T ; Kerzic, P J ; Irons, R D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c618t-7565c7d6eaec24fdda61b17e41320a2170baf16a48bcb5509ffe3cfc7e7b865a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Acute myeloid leukemia</topic><topic>Alkylation</topic><topic>Antigens, CD34</topic><topic>Benzene</topic><topic>Biological and medical sciences</topic><topic>Bone marrow</topic><topic>Bone Marrow Cells - cytology</topic><topic>Bone Marrow Cells - drug effects</topic><topic>Cancer Research</topic><topic>Carcinogens - pharmacology</topic><topic>CD34 antigen</topic><topic>Cell division</topic><topic>Cell Division - drug effects</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Chemotherapy</topic><topic>Colonies</topic><topic>Colony-stimulating factor</topic><topic>Critical Care Medicine</topic><topic>Cytokines</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Erythroleukemia</topic><topic>Extracellular signal-regulated kinase</topic><topic>Granulocyte-macrophage colony-stimulating factor</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - biosynthesis</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - metabolism</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology</topic><topic>Granulocytes</topic><topic>Health sciences</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hematology</topic><topic>Humans</topic><topic>Hydrocarbons</topic><topic>Hydroquinone</topic><topic>Hydroquinones - pharmacology</topic><topic>Intensive</topic><topic>Internal Medicine</topic><topic>Kinases</topic><topic>Kinetics</topic><topic>Leukemia</topic><topic>Leukemia, Erythroblastic, Acute - pathology</topic><topic>Leukemia, Myeloid, Acute - chemically induced</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic pathways</topic><topic>Metabolites</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Oncology</topic><topic>original-manuscript</topic><topic>Pathogenesis</topic><topic>Phosphorylation</topic><topic>Recombinant Proteins</topic><topic>Reporter gene</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><topic>Transcription activation</topic><topic>Transcription Factor AP-1 - metabolism</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zheng, J H</creatorcontrib><creatorcontrib>Pyatt, D W</creatorcontrib><creatorcontrib>Gross, S A</creatorcontrib><creatorcontrib>Le, A T</creatorcontrib><creatorcontrib>Kerzic, P 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human CD34+ bone marrow (BM) cells. The extracellular signal-regulated kinase (ERK) pathway plays an important role in GM-CSF-dependent proliferation and also has been implicated in the pathogenesis of acute myelogenous leukemia. Therefore, we investigated the effects of the benzene metabolite, hydroquinone (HQ), on alterations in the GM-CSF signaling pathway in TF-1 erythroleukemia cells and human CD34+ BM cells. HQ treatment in TF-1 cells results in a strong proliferative response that is dependent on ERK activation and GM-CSF production. HQ also induces ERK-dependent AP-1 activation with concomitant increased transcriptional activity of AP-1 reporter gene. However, the kinetics of ERK activation are different between rhGM-CSF and HQ in TF-1 cells: rhGM-CSF results in immediate activation of ERK, whereas HQ activation of ERK is delayed. Further, HQ and rhGM-CSF together produce an immediate increase in ERK phosphorylation, which is sustained for over 48 h. HQ also stimulates colony formation, AP-1 DNA binding and GM-CSF production in human CD34+ BM cells. These results suggest that HQ stimulates proliferation via activation of ERK/AP-1 and is at least partially mediated via the production of GM-CSF.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>15129224</pmid><doi>10.1038/sj.leu.2403389</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute myeloid leukemia Alkylation Antigens, CD34 Benzene Biological and medical sciences Bone marrow Bone Marrow Cells - cytology Bone Marrow Cells - drug effects Cancer Research Carcinogens - pharmacology CD34 antigen Cell division Cell Division - drug effects Cell Line, Tumor Cell proliferation Chemotherapy Colonies Colony-stimulating factor Critical Care Medicine Cytokines Deoxyribonucleic acid DNA Erythroleukemia Extracellular signal-regulated kinase Granulocyte-macrophage colony-stimulating factor Granulocyte-Macrophage Colony-Stimulating Factor - biosynthesis Granulocyte-Macrophage Colony-Stimulating Factor - metabolism Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology Granulocytes Health sciences Hematologic and hematopoietic diseases Hematology Humans Hydrocarbons Hydroquinone Hydroquinones - pharmacology Intensive Internal Medicine Kinases Kinetics Leukemia Leukemia, Erythroblastic, Acute - pathology Leukemia, Myeloid, Acute - chemically induced Medical sciences Medicine Medicine & Public Health Metabolic pathways Metabolites Mitogen-Activated Protein Kinases - metabolism Oncology original-manuscript Pathogenesis Phosphorylation Recombinant Proteins Reporter gene Signal transduction Signal Transduction - drug effects Signaling Transcription activation Transcription Factor AP-1 - metabolism Transcription factors |
| title | Hydroquinone modulates the GM-CSF signaling pathway in TF-1 cells |
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