Leukemia‐related transcription factor TEL/ETV6 expands erythroid precursors and stimulates hemoglobin synthesis
TEL/ETV6 located at chromosome 12p13 encodes a member of the E26 transformation‐specific family of transcription factors. TEL is known to be rearranged in a variety of leukemias and solid tumors resulting in the formation of oncogenic chimeric protein. Tel is essential for maintaining hematopoietic...
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| Veröffentlicht in: | Cancer science 2009-04, Vol.100 (4), p.689-697 |
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| creator | Eguchi‐Ishimae, Minenori Eguchi, Mariko Maki, Kazuhiro Porcher, Catherine Shimizu, Ritsuko Yamamoto, Masayuki Mitani, Kinuko |
| description | TEL/ETV6 located at chromosome 12p13 encodes a member of the E26 transformation‐specific family of transcription factors. TEL is known to be rearranged in a variety of leukemias and solid tumors resulting in the formation of oncogenic chimeric protein. Tel is essential for maintaining hematopoietic stem cells in the bone marrow. To understand the role of TEL in erythropoiesis, we generated transgenic mice expressing human TEL under the control of Gata1 promoter that is activated during the course of the erythroid‐lineage differentiation (GATA1‐TEL transgenic mice). Although GATA1‐TEL transgenic mice appeared healthy up to 18 months of age, the level of hemoglobin was higher in transgenic mice compared to non‐transgenic littermates. In addition, CD71+/TER119+ and c‐kit+/CD41+ populations proliferated with a higher frequency in transgenic mice when bone marrow cells were cultured in the presence of erythropoietin and thrombopoietin, respectively. In transgenic mice, enhanced expression of Alas‐e and β‐major globin genes was observed in erythroid‐committed cells. When embryonic stem cells expressing human TEL under the same Gata1 promoter were differentiated into hematopoietic cells, immature erythroid precursor increased better compared to controls as judged from the numbers of burst‐forming unit of erythrocytes. Our findings suggest some roles of TEL in expanding erythroid precursors and accumulating hemoglobin. (Cancer Sci 2009; 100: 689–697) |
| doi_str_mv | 10.1111/j.1349-7006.2009.01097.x |
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TEL is known to be rearranged in a variety of leukemias and solid tumors resulting in the formation of oncogenic chimeric protein. Tel is essential for maintaining hematopoietic stem cells in the bone marrow. To understand the role of TEL in erythropoiesis, we generated transgenic mice expressing human TEL under the control of Gata1 promoter that is activated during the course of the erythroid‐lineage differentiation (GATA1‐TEL transgenic mice). Although GATA1‐TEL transgenic mice appeared healthy up to 18 months of age, the level of hemoglobin was higher in transgenic mice compared to non‐transgenic littermates. In addition, CD71+/TER119+ and c‐kit+/CD41+ populations proliferated with a higher frequency in transgenic mice when bone marrow cells were cultured in the presence of erythropoietin and thrombopoietin, respectively. In transgenic mice, enhanced expression of Alas‐e and β‐major globin genes was observed in erythroid‐committed cells. When embryonic stem cells expressing human TEL under the same Gata1 promoter were differentiated into hematopoietic cells, immature erythroid precursor increased better compared to controls as judged from the numbers of burst‐forming unit of erythrocytes. Our findings suggest some roles of TEL in expanding erythroid precursors and accumulating hemoglobin. (Cancer Sci 2009; 100: 689–697)</description><identifier>ISSN: 1347-9032</identifier><identifier>ISSN: 1349-7006</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/j.1349-7006.2009.01097.x</identifier><identifier>PMID: 19302286</identifier><language>eng</language><publisher>Melbourne, Australia: Blackwell Publishing Asia</publisher><subject>Animals ; Biological and medical sciences ; Erythroid Precursor Cells - cytology ; Erythroid Precursor Cells - metabolism ; Erythropoiesis - genetics ; ETS Translocation Variant 6 Protein ; GATA1 Transcription Factor - genetics ; Hematologic and hematopoietic diseases ; Hemoglobins - biosynthesis ; Humans ; Leukemia - genetics ; Leukemias. Malignant lymphomas. Malignant reticulosis. 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TEL is known to be rearranged in a variety of leukemias and solid tumors resulting in the formation of oncogenic chimeric protein. Tel is essential for maintaining hematopoietic stem cells in the bone marrow. To understand the role of TEL in erythropoiesis, we generated transgenic mice expressing human TEL under the control of Gata1 promoter that is activated during the course of the erythroid‐lineage differentiation (GATA1‐TEL transgenic mice). Although GATA1‐TEL transgenic mice appeared healthy up to 18 months of age, the level of hemoglobin was higher in transgenic mice compared to non‐transgenic littermates. In addition, CD71+/TER119+ and c‐kit+/CD41+ populations proliferated with a higher frequency in transgenic mice when bone marrow cells were cultured in the presence of erythropoietin and thrombopoietin, respectively. In transgenic mice, enhanced expression of Alas‐e and β‐major globin genes was observed in erythroid‐committed cells. When embryonic stem cells expressing human TEL under the same Gata1 promoter were differentiated into hematopoietic cells, immature erythroid precursor increased better compared to controls as judged from the numbers of burst‐forming unit of erythrocytes. Our findings suggest some roles of TEL in expanding erythroid precursors and accumulating hemoglobin. (Cancer Sci 2009; 100: 689–697)</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Erythroid Precursor Cells - cytology</subject><subject>Erythroid Precursor Cells - metabolism</subject><subject>Erythropoiesis - genetics</subject><subject>ETS Translocation Variant 6 Protein</subject><subject>GATA1 Transcription Factor - genetics</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hemoglobins - biosynthesis</subject><subject>Humans</subject><subject>Leukemia - genetics</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Original</subject><subject>Promoter Regions, Genetic</subject><subject>Proto-Oncogene Proteins c-ets - genetics</subject><subject>Repressor Proteins - genetics</subject><subject>Tumors</subject><issn>1347-9032</issn><issn>1349-7006</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhSNERUvhFZA3sEvqn4ydLBCqRsOPNFIXHdhajnOn4yGJU9-kzOx4BJ6RJ8HpjAa6wxtf63z3-NonSQijGYvrapsxkZepolRmnNIyo4yWKts9Sy5OwvPHWqUlFfw8eYm4pVTIvMxfJOesFJTzQl4k90sYv0PrzO-fvwI0ZoCaDMF0aIPrB-c7sjZ28IGsFsurxeqbJLDrTVcjgbAfNsG7mvQB7BjQByRRITi4dpyckGyg9XeNr1xHcN8NG0CHr5KztWkQXh_3y-Trx8Vq_jld3nz6Mr9eplZyrtJKSsrivEZZVRdc5JaqEpSpc1XQGVdlxVk81VBZUxtqlBI1nSlmoyqEFOIy-XDw7ceqhdpCF9_V6D641oS99sbpp0rnNvrOP-j4wbNCcRYd3h0dgr8fAQfdOrTQNKYDP6KWis9yJlQEiwNog0cMsD7dwuhkx_RWT7noKRc9BaYfA9O72Prm3yn_Nh4TisDbI2DQmmYds7EOT1wcU0gmaeTeH7gfroH9fw-g59e3UyX-ABvZtR0</recordid><startdate>200904</startdate><enddate>200904</enddate><creator>Eguchi‐Ishimae, Minenori</creator><creator>Eguchi, Mariko</creator><creator>Maki, Kazuhiro</creator><creator>Porcher, Catherine</creator><creator>Shimizu, Ritsuko</creator><creator>Yamamoto, Masayuki</creator><creator>Mitani, Kinuko</creator><general>Blackwell Publishing Asia</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><scope>5PM</scope></search><sort><creationdate>200904</creationdate><title>Leukemia‐related transcription factor TEL/ETV6 expands erythroid precursors and stimulates hemoglobin synthesis</title><author>Eguchi‐Ishimae, Minenori ; Eguchi, Mariko ; Maki, Kazuhiro ; Porcher, Catherine ; Shimizu, Ritsuko ; Yamamoto, Masayuki ; Mitani, Kinuko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6227-b6601364a7c7d8234c079e7ad47805279b217addebcada0a773d0571c80533633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Erythroid Precursor Cells - cytology</topic><topic>Erythroid Precursor Cells - metabolism</topic><topic>Erythropoiesis - genetics</topic><topic>ETS Translocation Variant 6 Protein</topic><topic>GATA1 Transcription Factor - genetics</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hemoglobins - biosynthesis</topic><topic>Humans</topic><topic>Leukemia - genetics</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Original</topic><topic>Promoter Regions, Genetic</topic><topic>Proto-Oncogene Proteins c-ets - genetics</topic><topic>Repressor Proteins - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eguchi‐Ishimae, Minenori</creatorcontrib><creatorcontrib>Eguchi, Mariko</creatorcontrib><creatorcontrib>Maki, Kazuhiro</creatorcontrib><creatorcontrib>Porcher, Catherine</creatorcontrib><creatorcontrib>Shimizu, Ritsuko</creatorcontrib><creatorcontrib>Yamamoto, Masayuki</creatorcontrib><creatorcontrib>Mitani, Kinuko</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Eguchi‐Ishimae, Minenori</au><au>Eguchi, Mariko</au><au>Maki, Kazuhiro</au><au>Porcher, Catherine</au><au>Shimizu, Ritsuko</au><au>Yamamoto, Masayuki</au><au>Mitani, Kinuko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Leukemia‐related transcription factor TEL/ETV6 expands erythroid precursors and stimulates hemoglobin synthesis</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2009-04</date><risdate>2009</risdate><volume>100</volume><issue>4</issue><spage>689</spage><epage>697</epage><pages>689-697</pages><issn>1347-9032</issn><issn>1349-7006</issn><eissn>1349-7006</eissn><abstract>TEL/ETV6 located at chromosome 12p13 encodes a member of the E26 transformation‐specific family of transcription factors. TEL is known to be rearranged in a variety of leukemias and solid tumors resulting in the formation of oncogenic chimeric protein. Tel is essential for maintaining hematopoietic stem cells in the bone marrow. To understand the role of TEL in erythropoiesis, we generated transgenic mice expressing human TEL under the control of Gata1 promoter that is activated during the course of the erythroid‐lineage differentiation (GATA1‐TEL transgenic mice). Although GATA1‐TEL transgenic mice appeared healthy up to 18 months of age, the level of hemoglobin was higher in transgenic mice compared to non‐transgenic littermates. In addition, CD71+/TER119+ and c‐kit+/CD41+ populations proliferated with a higher frequency in transgenic mice when bone marrow cells were cultured in the presence of erythropoietin and thrombopoietin, respectively. In transgenic mice, enhanced expression of Alas‐e and β‐major globin genes was observed in erythroid‐committed cells. When embryonic stem cells expressing human TEL under the same Gata1 promoter were differentiated into hematopoietic cells, immature erythroid precursor increased better compared to controls as judged from the numbers of burst‐forming unit of erythrocytes. Our findings suggest some roles of TEL in expanding erythroid precursors and accumulating hemoglobin. (Cancer Sci 2009; 100: 689–697)</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Publishing Asia</pub><pmid>19302286</pmid><doi>10.1111/j.1349-7006.2009.01097.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancer science, 2009-04, Vol.100 (4), p.689-697 |
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| subjects | Animals Biological and medical sciences Erythroid Precursor Cells - cytology Erythroid Precursor Cells - metabolism Erythropoiesis - genetics ETS Translocation Variant 6 Protein GATA1 Transcription Factor - genetics Hematologic and hematopoietic diseases Hemoglobins - biosynthesis Humans Leukemia - genetics Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Mice Mice, Transgenic Original Promoter Regions, Genetic Proto-Oncogene Proteins c-ets - genetics Repressor Proteins - genetics Tumors |
| title | Leukemia‐related transcription factor TEL/ETV6 expands erythroid precursors and stimulates hemoglobin synthesis |
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