Interferon α extends the survival of human myeloma cells through an upregulation of the Mcl‐1 anti‐apoptotic molecule
We have recently reported that Mcl‐1, an anti‐apoptotic member of the Bcl‐2 family, is upregulated by interleukin (IL)‐6 in human myeloma cells through the janus kinase/signal transducers and activators of transduction (JAK/STAT) pathway. In the current study, we have explored the effects of interfe...
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| Veröffentlicht in: | British journal of haematology 2001-02, Vol.112 (2), p.358-363 |
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| container_title | British journal of haematology |
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| creator | Puthier, Denis Thabard, Wilfrid Rapp, Marie‐José Etrillard, Marguerite Harousseau, Jean‐Luc Bataille, Régis Amiot, Martine |
| description | We have recently reported that Mcl‐1, an anti‐apoptotic member of the Bcl‐2 family, is upregulated by interleukin (IL)‐6 in human myeloma cells through the janus kinase/signal transducers and activators of transduction (JAK/STAT) pathway. In the current study, we have explored the effects of interferon (IFN)‐α, a cytokine which has been shown to increase myeloma cell survival. Our results demonstrate that IFN‐α potently upregulates Mcl‐1 on both myeloma cell lines and purified native myeloma cells. Of note, this upregulation is not due to an induction of an IL‐6 autocrine loop. Furthermore, we showed that IL‐6 and IFN‐α had no additive effect on Mcl‐1 upregulation, suggesting that both cytokines act through a common mechanism. Finally, the analysis of signalling transduction pathways strongly suggests that Mcl‐1 upregulation induced by IFN‐α depends on STAT3 activation. Altogether, our data show that IFN‐α has an IL‐6‐like effect on human myeloma cells and suggest that it could be deleterious in some patients. |
| doi_str_mv | 10.1046/j.1365-2141.2001.02575.x |
| format | Article |
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In the current study, we have explored the effects of interferon (IFN)‐α, a cytokine which has been shown to increase myeloma cell survival. Our results demonstrate that IFN‐α potently upregulates Mcl‐1 on both myeloma cell lines and purified native myeloma cells. Of note, this upregulation is not due to an induction of an IL‐6 autocrine loop. Furthermore, we showed that IL‐6 and IFN‐α had no additive effect on Mcl‐1 upregulation, suggesting that both cytokines act through a common mechanism. Finally, the analysis of signalling transduction pathways strongly suggests that Mcl‐1 upregulation induced by IFN‐α depends on STAT3 activation. Altogether, our data show that IFN‐α has an IL‐6‐like effect on human myeloma cells and suggest that it could be deleterious in some patients.</description><identifier>ISSN: 0007-1048</identifier><identifier>EISSN: 1365-2141</identifier><identifier>DOI: 10.1046/j.1365-2141.2001.02575.x</identifier><identifier>PMID: 11167829</identifier><identifier>CODEN: BJHEAL</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Antineoplastic agents ; Apoptosis ; Biological and medical sciences ; Chemotherapy ; DNA-Binding Proteins - metabolism ; Humans ; IFN‐α ; IL‐6 ; Interferon-alpha - pharmacology ; Interleukin-6 - metabolism ; Mcl‐1 ; Medical sciences ; multiple myeloma ; Multiple Myeloma - metabolism ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins - metabolism ; Pharmacology. Drug treatments ; Proto-Oncogene Proteins c-bcl-2 ; Signal Transduction ; STAT3 ; STAT3 Transcription Factor ; Trans-Activators - metabolism ; Tumor Cells, Cultured</subject><ispartof>British journal of haematology, 2001-02, Vol.112 (2), p.358-363</ispartof><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4435-e5270d51fb640809dfdfb400340bd129eef9ef3fbcdef736db6f6ce71a1771e63</citedby><cites>FETCH-LOGICAL-c4435-e5270d51fb640809dfdfb400340bd129eef9ef3fbcdef736db6f6ce71a1771e63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1365-2141.2001.02575.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1365-2141.2001.02575.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=977110$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11167829$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Puthier, Denis</creatorcontrib><creatorcontrib>Thabard, Wilfrid</creatorcontrib><creatorcontrib>Rapp, Marie‐José</creatorcontrib><creatorcontrib>Etrillard, Marguerite</creatorcontrib><creatorcontrib>Harousseau, Jean‐Luc</creatorcontrib><creatorcontrib>Bataille, Régis</creatorcontrib><creatorcontrib>Amiot, Martine</creatorcontrib><title>Interferon α extends the survival of human myeloma cells through an upregulation of the Mcl‐1 anti‐apoptotic molecule</title><title>British journal of haematology</title><addtitle>Br J Haematol</addtitle><description>We have recently reported that Mcl‐1, an anti‐apoptotic member of the Bcl‐2 family, is upregulated by interleukin (IL)‐6 in human myeloma cells through the janus kinase/signal transducers and activators of transduction (JAK/STAT) pathway. In the current study, we have explored the effects of interferon (IFN)‐α, a cytokine which has been shown to increase myeloma cell survival. Our results demonstrate that IFN‐α potently upregulates Mcl‐1 on both myeloma cell lines and purified native myeloma cells. Of note, this upregulation is not due to an induction of an IL‐6 autocrine loop. Furthermore, we showed that IL‐6 and IFN‐α had no additive effect on Mcl‐1 upregulation, suggesting that both cytokines act through a common mechanism. Finally, the analysis of signalling transduction pathways strongly suggests that Mcl‐1 upregulation induced by IFN‐α depends on STAT3 activation. Altogether, our data show that IFN‐α has an IL‐6‐like effect on human myeloma cells and suggest that it could be deleterious in some patients.</description><subject>Antineoplastic agents</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Chemotherapy</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Humans</subject><subject>IFN‐α</subject><subject>IL‐6</subject><subject>Interferon-alpha - pharmacology</subject><subject>Interleukin-6 - metabolism</subject><subject>Mcl‐1</subject><subject>Medical sciences</subject><subject>multiple myeloma</subject><subject>Multiple Myeloma - metabolism</subject><subject>Myeloid Cell Leukemia Sequence 1 Protein</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Proto-Oncogene Proteins c-bcl-2</subject><subject>Signal Transduction</subject><subject>STAT3</subject><subject>STAT3 Transcription Factor</subject><subject>Trans-Activators - metabolism</subject><subject>Tumor Cells, Cultured</subject><issn>0007-1048</issn><issn>1365-2141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE2O1DAQRi0EYpqBKyBLSOwSXPmxkwULGAEzaBAbWFuOU55Oy4mDHQ_drDgCV-EiHIKT4NCtYcvKJdX7qsqPEAosB1bxF7scSl5nBVSQF4xBzopa1Pn-HtncNe6TDWNMZCnQnJFHIewSWLIaHpIzAOCiKdoN-XY1LegNejfRXz8p7hec-kCXLdIQ_e1wqyx1hm7jqCY6HtC6UVGN1q6Md_FmS1Mjzh5volXLkMYkfI1_0Pb39x-Q2suQCjW7eXHLoOnoLOpo8TF5YJQN-OT0npPPb998urjMrj--u7p4dZ3pqirrDOtCsL4G0_GKNaztTW-6irGyYl0PRYtoWjSl6XSPRpS877jhGgUoEAKQl-fk-XHu7N2XiGGR4xDWL6gJXQxSMF6U0NQJbI6g9i4Ej0bOfhiVP0hgcvUud3LVK1e9cvUu_3qX-xR9etoRuxH7f8GT6AQ8OwEqaGWNV5Mewh3XplOBJerlkfo6WDz893r5-v3lWpV_ALwKosY</recordid><startdate>200102</startdate><enddate>200102</enddate><creator>Puthier, Denis</creator><creator>Thabard, Wilfrid</creator><creator>Rapp, Marie‐José</creator><creator>Etrillard, Marguerite</creator><creator>Harousseau, Jean‐Luc</creator><creator>Bataille, Régis</creator><creator>Amiot, Martine</creator><general>Blackwell Science Ltd</general><general>Blackwell</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>200102</creationdate><title>Interferon α extends the survival of human myeloma cells through an upregulation of the Mcl‐1 anti‐apoptotic molecule</title><author>Puthier, Denis ; Thabard, Wilfrid ; Rapp, Marie‐José ; Etrillard, Marguerite ; Harousseau, Jean‐Luc ; Bataille, Régis ; Amiot, Martine</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4435-e5270d51fb640809dfdfb400340bd129eef9ef3fbcdef736db6f6ce71a1771e63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Antineoplastic agents</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Chemotherapy</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Humans</topic><topic>IFN‐α</topic><topic>IL‐6</topic><topic>Interferon-alpha - pharmacology</topic><topic>Interleukin-6 - metabolism</topic><topic>Mcl‐1</topic><topic>Medical sciences</topic><topic>multiple myeloma</topic><topic>Multiple Myeloma - metabolism</topic><topic>Myeloid Cell Leukemia Sequence 1 Protein</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Proto-Oncogene Proteins c-bcl-2</topic><topic>Signal Transduction</topic><topic>STAT3</topic><topic>STAT3 Transcription Factor</topic><topic>Trans-Activators - metabolism</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Puthier, Denis</creatorcontrib><creatorcontrib>Thabard, Wilfrid</creatorcontrib><creatorcontrib>Rapp, Marie‐José</creatorcontrib><creatorcontrib>Etrillard, Marguerite</creatorcontrib><creatorcontrib>Harousseau, Jean‐Luc</creatorcontrib><creatorcontrib>Bataille, Régis</creatorcontrib><creatorcontrib>Amiot, Martine</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>British journal of haematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Puthier, Denis</au><au>Thabard, Wilfrid</au><au>Rapp, Marie‐José</au><au>Etrillard, Marguerite</au><au>Harousseau, Jean‐Luc</au><au>Bataille, Régis</au><au>Amiot, Martine</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interferon α extends the survival of human myeloma cells through an upregulation of the Mcl‐1 anti‐apoptotic molecule</atitle><jtitle>British journal of haematology</jtitle><addtitle>Br J Haematol</addtitle><date>2001-02</date><risdate>2001</risdate><volume>112</volume><issue>2</issue><spage>358</spage><epage>363</epage><pages>358-363</pages><issn>0007-1048</issn><eissn>1365-2141</eissn><coden>BJHEAL</coden><abstract>We have recently reported that Mcl‐1, an anti‐apoptotic member of the Bcl‐2 family, is upregulated by interleukin (IL)‐6 in human myeloma cells through the janus kinase/signal transducers and activators of transduction (JAK/STAT) pathway. In the current study, we have explored the effects of interferon (IFN)‐α, a cytokine which has been shown to increase myeloma cell survival. Our results demonstrate that IFN‐α potently upregulates Mcl‐1 on both myeloma cell lines and purified native myeloma cells. Of note, this upregulation is not due to an induction of an IL‐6 autocrine loop. Furthermore, we showed that IL‐6 and IFN‐α had no additive effect on Mcl‐1 upregulation, suggesting that both cytokines act through a common mechanism. Finally, the analysis of signalling transduction pathways strongly suggests that Mcl‐1 upregulation induced by IFN‐α depends on STAT3 activation. Altogether, our data show that IFN‐α has an IL‐6‐like effect on human myeloma cells and suggest that it could be deleterious in some patients.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>11167829</pmid><doi>10.1046/j.1365-2141.2001.02575.x</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antineoplastic agents Apoptosis Biological and medical sciences Chemotherapy DNA-Binding Proteins - metabolism Humans IFN‐α IL‐6 Interferon-alpha - pharmacology Interleukin-6 - metabolism Mcl‐1 Medical sciences multiple myeloma Multiple Myeloma - metabolism Myeloid Cell Leukemia Sequence 1 Protein Neoplasm Proteins - metabolism Pharmacology. Drug treatments Proto-Oncogene Proteins c-bcl-2 Signal Transduction STAT3 STAT3 Transcription Factor Trans-Activators - metabolism Tumor Cells, Cultured |
| title | Interferon α extends the survival of human myeloma cells through an upregulation of the Mcl‐1 anti‐apoptotic molecule |
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