Id1 transcription inhibitor-matrix metalloproteinase 9 axis enhances invasiveness of the breakpoint cluster region/abelson tyrosine kinase-transformed leukemia cells
Breakpoint cluster region/Abelson (BCR/ABL) tyrosine kinase enhances the ability of leukemia cells to infiltrate various organs. We show here that expression of the helix-loop-helix transcription factor Id1 is enhanced by BCR/ABL in a signal transducer and activator of transcription 5 (STAT5)-depend...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2006-04, Vol.66 (8), p.4108-4116 |
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| container_title | Cancer research (Chicago, Ill.) |
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| creator | NIEBOROWSKA-SKORSKA, Margaret HOSER, Grazyna RINK, Lori MALECKI, Maciej KOSSEV, Plamen WASIK, Mariusz A SKORSKI, Tomasz |
| description | Breakpoint cluster region/Abelson (BCR/ABL) tyrosine kinase enhances the ability of leukemia cells to infiltrate various organs. We show here that expression of the helix-loop-helix transcription factor Id1 is enhanced by BCR/ABL in a signal transducer and activator of transcription 5 (STAT5)-dependent manner. Enhanced expression of Id1 plays a key role in BCR/ABL-mediated cell invasion. Down-regulation of Id1 in BCR/ABL leukemia cells by the antisense cDNA significantly reduced their invasive capability through the Matrigel membrane and their ability to infiltrate hematopoietic and nonhematopoietic organs resulting in delayed leukemogenesis in mice. The Id1-promoted cell invasiveness was seemingly mediated by matrix metalloproteinase 9 (MMP9). Transactivation of MMP9 promoter in BCR/ABL cells was dependent on Id1 and abrogation of the MMP9 catalytic activity by a metalloproteinase inhibitor or blocking antibody decreased invasive capacity of leukemia cells. These data suggest that BCR/ABL-STAT5-Id1-MMP9 pathway may play a critical role in BCR/ABL-mediated leukemogenesis by enhancing invasiveness of leukemia cells. |
| doi_str_mv | 10.1158/0008-5472.CAN-05-1584 |
| format | Article |
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We show here that expression of the helix-loop-helix transcription factor Id1 is enhanced by BCR/ABL in a signal transducer and activator of transcription 5 (STAT5)-dependent manner. Enhanced expression of Id1 plays a key role in BCR/ABL-mediated cell invasion. Down-regulation of Id1 in BCR/ABL leukemia cells by the antisense cDNA significantly reduced their invasive capability through the Matrigel membrane and their ability to infiltrate hematopoietic and nonhematopoietic organs resulting in delayed leukemogenesis in mice. The Id1-promoted cell invasiveness was seemingly mediated by matrix metalloproteinase 9 (MMP9). Transactivation of MMP9 promoter in BCR/ABL cells was dependent on Id1 and abrogation of the MMP9 catalytic activity by a metalloproteinase inhibitor or blocking antibody decreased invasive capacity of leukemia cells. These data suggest that BCR/ABL-STAT5-Id1-MMP9 pathway may play a critical role in BCR/ABL-mediated leukemogenesis by enhancing invasiveness of leukemia cells.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-05-1584</identifier><identifier>PMID: 16618731</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Antineoplastic agents ; Biological and medical sciences ; Cell Transformation, Neoplastic - metabolism ; Fusion Proteins, bcr-abl ; Hematologic and hematopoietic diseases ; Hematopoietic Stem Cells - metabolism ; Hematopoietic Stem Cells - physiology ; Inhibitor of Differentiation Protein 1 - biosynthesis ; Inhibitor of Differentiation Protein 1 - genetics ; Inhibitor of Differentiation Protein 1 - metabolism ; Leukemia, Experimental - enzymology ; Leukemia, Experimental - genetics ; Leukemia, Experimental - pathology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Matrix Metalloproteinase 9 - metabolism ; Medical sciences ; Mice ; Mice, SCID ; Neoplasm Invasiveness ; Pharmacology. Drug treatments ; Promoter Regions, Genetic ; Protein-Tyrosine Kinases - genetics ; Protein-Tyrosine Kinases - metabolism ; STAT5 Transcription Factor - metabolism ; Transcriptional Activation ; Tumors</subject><ispartof>Cancer research (Chicago, Ill.), 2006-04, Vol.66 (8), p.4108-4116</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-5fc0cd5c163dc48f82cc5a8fddde38ec3b9f03a538998cc5a6132b72b869c06e3</citedby><cites>FETCH-LOGICAL-c448t-5fc0cd5c163dc48f82cc5a8fddde38ec3b9f03a538998cc5a6132b72b869c06e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,3345,27907,27908</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17699915$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16618731$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NIEBOROWSKA-SKORSKA, Margaret</creatorcontrib><creatorcontrib>HOSER, Grazyna</creatorcontrib><creatorcontrib>RINK, Lori</creatorcontrib><creatorcontrib>MALECKI, Maciej</creatorcontrib><creatorcontrib>KOSSEV, Plamen</creatorcontrib><creatorcontrib>WASIK, Mariusz A</creatorcontrib><creatorcontrib>SKORSKI, Tomasz</creatorcontrib><title>Id1 transcription inhibitor-matrix metalloproteinase 9 axis enhances invasiveness of the breakpoint cluster region/abelson tyrosine kinase-transformed leukemia cells</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Breakpoint cluster region/Abelson (BCR/ABL) tyrosine kinase enhances the ability of leukemia cells to infiltrate various organs. We show here that expression of the helix-loop-helix transcription factor Id1 is enhanced by BCR/ABL in a signal transducer and activator of transcription 5 (STAT5)-dependent manner. Enhanced expression of Id1 plays a key role in BCR/ABL-mediated cell invasion. Down-regulation of Id1 in BCR/ABL leukemia cells by the antisense cDNA significantly reduced their invasive capability through the Matrigel membrane and their ability to infiltrate hematopoietic and nonhematopoietic organs resulting in delayed leukemogenesis in mice. The Id1-promoted cell invasiveness was seemingly mediated by matrix metalloproteinase 9 (MMP9). Transactivation of MMP9 promoter in BCR/ABL cells was dependent on Id1 and abrogation of the MMP9 catalytic activity by a metalloproteinase inhibitor or blocking antibody decreased invasive capacity of leukemia cells. These data suggest that BCR/ABL-STAT5-Id1-MMP9 pathway may play a critical role in BCR/ABL-mediated leukemogenesis by enhancing invasiveness of leukemia cells.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Fusion Proteins, bcr-abl</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hematopoietic Stem Cells - metabolism</subject><subject>Hematopoietic Stem Cells - physiology</subject><subject>Inhibitor of Differentiation Protein 1 - biosynthesis</subject><subject>Inhibitor of Differentiation Protein 1 - genetics</subject><subject>Inhibitor of Differentiation Protein 1 - metabolism</subject><subject>Leukemia, Experimental - enzymology</subject><subject>Leukemia, Experimental - genetics</subject><subject>Leukemia, Experimental - pathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, SCID</subject><subject>Neoplasm Invasiveness</subject><subject>Pharmacology. Drug treatments</subject><subject>Promoter Regions, Genetic</subject><subject>Protein-Tyrosine Kinases - genetics</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>STAT5 Transcription Factor - metabolism</subject><subject>Transcriptional Activation</subject><subject>Tumors</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks9u1DAQxi0EokvhEUC-wM2tvY4T51it-FOpggucLccZs2YdZ_E4VftAvCdOu6JHTpY9v5lvZj4T8lbwCyGUvuSca6aabnuxu_rKuGL1sXlGNkJJzbqmUc_J5h9zRl4h_qpXJbh6Sc5E2wrdSbEhf65HQUu2CV0OxxLmREPahyGUObPJlhzu6ATFxjgf81wgJItAe2rvAlJIe5scYE25tRhuIQEinT0te6BDBns4ziEV6uKCBTLN8LMKXNoBIlahcp9nDAno4aEqe2jDz3mCkUZYDjAFSx3EiK_JC28jwpvTeU5-fPr4ffeF3Xz7fL27umGuaXRhyjvuRuVEK0fXaK-3zimr_TiOIDU4OfSeS1s31Pd6DbVCboduO-i2d7wFeU4-PNats_5eAIuZAq4d2ATzgqbttNJSNv8FRScaoXpVQfUIujorZvDmmMNk870R3KxGmtUks5pkqpGGK7MaWfPenQSWoe7jKevkXAXenwCLzkZfd-cCPnFd2_d9_Qx_AYUWrFA</recordid><startdate>20060415</startdate><enddate>20060415</enddate><creator>NIEBOROWSKA-SKORSKA, Margaret</creator><creator>HOSER, Grazyna</creator><creator>RINK, Lori</creator><creator>MALECKI, Maciej</creator><creator>KOSSEV, Plamen</creator><creator>WASIK, Mariusz A</creator><creator>SKORSKI, Tomasz</creator><general>American Association for Cancer Research</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>7TM</scope><scope>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20060415</creationdate><title>Id1 transcription inhibitor-matrix metalloproteinase 9 axis enhances invasiveness of the breakpoint cluster region/abelson tyrosine kinase-transformed leukemia cells</title><author>NIEBOROWSKA-SKORSKA, Margaret ; HOSER, Grazyna ; RINK, Lori ; MALECKI, Maciej ; KOSSEV, Plamen ; WASIK, Mariusz A ; SKORSKI, Tomasz</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-5fc0cd5c163dc48f82cc5a8fddde38ec3b9f03a538998cc5a6132b72b869c06e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Fusion Proteins, bcr-abl</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hematopoietic Stem Cells - metabolism</topic><topic>Hematopoietic Stem Cells - physiology</topic><topic>Inhibitor of Differentiation Protein 1 - biosynthesis</topic><topic>Inhibitor of Differentiation Protein 1 - genetics</topic><topic>Inhibitor of Differentiation Protein 1 - metabolism</topic><topic>Leukemia, Experimental - enzymology</topic><topic>Leukemia, Experimental - genetics</topic><topic>Leukemia, Experimental - pathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, SCID</topic><topic>Neoplasm Invasiveness</topic><topic>Pharmacology. Drug treatments</topic><topic>Promoter Regions, Genetic</topic><topic>Protein-Tyrosine Kinases - genetics</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>STAT5 Transcription Factor - metabolism</topic><topic>Transcriptional Activation</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NIEBOROWSKA-SKORSKA, Margaret</creatorcontrib><creatorcontrib>HOSER, Grazyna</creatorcontrib><creatorcontrib>RINK, Lori</creatorcontrib><creatorcontrib>MALECKI, Maciej</creatorcontrib><creatorcontrib>KOSSEV, Plamen</creatorcontrib><creatorcontrib>WASIK, Mariusz A</creatorcontrib><creatorcontrib>SKORSKI, Tomasz</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>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NIEBOROWSKA-SKORSKA, Margaret</au><au>HOSER, Grazyna</au><au>RINK, Lori</au><au>MALECKI, Maciej</au><au>KOSSEV, Plamen</au><au>WASIK, Mariusz A</au><au>SKORSKI, Tomasz</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Id1 transcription inhibitor-matrix metalloproteinase 9 axis enhances invasiveness of the breakpoint cluster region/abelson tyrosine kinase-transformed leukemia cells</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2006-04-15</date><risdate>2006</risdate><volume>66</volume><issue>8</issue><spage>4108</spage><epage>4116</epage><pages>4108-4116</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Breakpoint cluster region/Abelson (BCR/ABL) tyrosine kinase enhances the ability of leukemia cells to infiltrate various organs. We show here that expression of the helix-loop-helix transcription factor Id1 is enhanced by BCR/ABL in a signal transducer and activator of transcription 5 (STAT5)-dependent manner. Enhanced expression of Id1 plays a key role in BCR/ABL-mediated cell invasion. Down-regulation of Id1 in BCR/ABL leukemia cells by the antisense cDNA significantly reduced their invasive capability through the Matrigel membrane and their ability to infiltrate hematopoietic and nonhematopoietic organs resulting in delayed leukemogenesis in mice. The Id1-promoted cell invasiveness was seemingly mediated by matrix metalloproteinase 9 (MMP9). Transactivation of MMP9 promoter in BCR/ABL cells was dependent on Id1 and abrogation of the MMP9 catalytic activity by a metalloproteinase inhibitor or blocking antibody decreased invasive capacity of leukemia cells. These data suggest that BCR/ABL-STAT5-Id1-MMP9 pathway may play a critical role in BCR/ABL-mediated leukemogenesis by enhancing invasiveness of leukemia cells.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>16618731</pmid><doi>10.1158/0008-5472.CAN-05-1584</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Antineoplastic agents Biological and medical sciences Cell Transformation, Neoplastic - metabolism Fusion Proteins, bcr-abl Hematologic and hematopoietic diseases Hematopoietic Stem Cells - metabolism Hematopoietic Stem Cells - physiology Inhibitor of Differentiation Protein 1 - biosynthesis Inhibitor of Differentiation Protein 1 - genetics Inhibitor of Differentiation Protein 1 - metabolism Leukemia, Experimental - enzymology Leukemia, Experimental - genetics Leukemia, Experimental - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Matrix Metalloproteinase 9 - metabolism Medical sciences Mice Mice, SCID Neoplasm Invasiveness Pharmacology. Drug treatments Promoter Regions, Genetic Protein-Tyrosine Kinases - genetics Protein-Tyrosine Kinases - metabolism STAT5 Transcription Factor - metabolism Transcriptional Activation Tumors |
| title | Id1 transcription inhibitor-matrix metalloproteinase 9 axis enhances invasiveness of the breakpoint cluster region/abelson tyrosine kinase-transformed leukemia cells |
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