Establishment and characterization of a unique human cell line that proliferates dependently on GM-CSF, IL-3, or erythropoietin

We have established a novel cell line, designated as TF‐1, from a patient with erythroleukemia, which showed complete growth dependency on granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) or on interleukin‐3 (IL‐3) and carried a homogeneous chromosomal abnormality (54X). Erythropoietin (EPO...

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Veröffentlicht in:Journal of cellular physiology 1989-08, Vol.140 (2), p.323-334
Hauptverfasser: Kitamura, Toshio, Tange, Tsuyoshi, Terasawa, Takashi, Chiba, Shigeru, Kuwaki, Tomoaki, Miyagawa, Kiyoshi, Piao, Yun-Feng, Miyazono, Kohei, Urabe, Akio, Takaku, Fumimaro
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container_issue 2
container_start_page 323
container_title Journal of cellular physiology
container_volume 140
creator Kitamura, Toshio
Tange, Tsuyoshi
Terasawa, Takashi
Chiba, Shigeru
Kuwaki, Tomoaki
Miyagawa, Kiyoshi
Piao, Yun-Feng
Miyazono, Kohei
Urabe, Akio
Takaku, Fumimaro
description We have established a novel cell line, designated as TF‐1, from a patient with erythroleukemia, which showed complete growth dependency on granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) or on interleukin‐3 (IL‐3) and carried a homogeneous chromosomal abnormality (54X). Erythropoietin (EPO) also sustained the short‐term growth of TF‐1, but did not induce erythroid differentiation. These three hematopoietic growth factors acted on TF‐1 synergistically. Transforming growth factorβ and interferons inhibited the factor‐dependent growth of TF‐1 cells in a dose‐dependent fashion, and monocyte‐colony stimulating factor and interkeukin‐1 enhanced the GM‐CSF‐dependent growth of TF‐1. Ultrastructural studies revealed some very immature features in this cell line. Although TF‐1 cells do not express glycophorin A or carbonyl anhydrase I, the morphological and cytochemical features, and the constitutive expression of globin genes, indicate the commitment of TF‐1 to erythroid lineage. When induced to differentiate, TF‐1 entered two different pathways. Specifically, hemin and delta‐arninolevulinic acid induced hemoglobin synthesis, whereas TPA induced dramatic differentiation of TF‐1 into macrophage‐like cells. In summary, TF‐1 is a cell lineof immature erythroid origin that requires GM‐CSF, IL‐3, or EPO for its growth and that has the ability to undergo differentiation into either more mature erythroid cells or into macrophage‐like cells. TF‐1 is auseful tool for analyzing the human receptors for IL‐3, GM‐CSF, and EPO or the signal transduction of these hemopoietic growth factors.
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Cell. Physiol</addtitle><description>We have established a novel cell line, designated as TF‐1, from a patient with erythroleukemia, which showed complete growth dependency on granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) or on interleukin‐3 (IL‐3) and carried a homogeneous chromosomal abnormality (54X). Erythropoietin (EPO) also sustained the short‐term growth of TF‐1, but did not induce erythroid differentiation. These three hematopoietic growth factors acted on TF‐1 synergistically. Transforming growth factorβ and interferons inhibited the factor‐dependent growth of TF‐1 cells in a dose‐dependent fashion, and monocyte‐colony stimulating factor and interkeukin‐1 enhanced the GM‐CSF‐dependent growth of TF‐1. Ultrastructural studies revealed some very immature features in this cell line. Although TF‐1 cells do not express glycophorin A or carbonyl anhydrase I, the morphological and cytochemical features, and the constitutive expression of globin genes, indicate the commitment of TF‐1 to erythroid lineage. When induced to differentiate, TF‐1 entered two different pathways. Specifically, hemin and delta‐arninolevulinic acid induced hemoglobin synthesis, whereas TPA induced dramatic differentiation of TF‐1 into macrophage‐like cells. In summary, TF‐1 is a cell lineof immature erythroid origin that requires GM‐CSF, IL‐3, or EPO for its growth and that has the ability to undergo differentiation into either more mature erythroid cells or into macrophage‐like cells. 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Hybridization. Fusion</topic><topic>Cell Line</topic><topic>Cell Transformation, Neoplastic - drug effects</topic><topic>Colony-Stimulating Factors - pharmacology</topic><topic>Erythropoietin - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor</topic><topic>Growth Substances - pharmacology</topic><topic>Humans</topic><topic>Interleukin-3 - pharmacology</topic><topic>Leukemia, Erythroblastic, Acute - pathology</topic><topic>Male</topic><topic>Mitosis</topic><topic>Molecular and cellular biology</topic><topic>Stem Cells - pathology</topic><topic>Tumor Cells, Cultured - analysis</topic><topic>Tumor Cells, Cultured - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kitamura, Toshio</creatorcontrib><creatorcontrib>Tange, Tsuyoshi</creatorcontrib><creatorcontrib>Terasawa, Takashi</creatorcontrib><creatorcontrib>Chiba, Shigeru</creatorcontrib><creatorcontrib>Kuwaki, Tomoaki</creatorcontrib><creatorcontrib>Miyagawa, Kiyoshi</creatorcontrib><creatorcontrib>Piao, Yun-Feng</creatorcontrib><creatorcontrib>Miyazono, Kohei</creatorcontrib><creatorcontrib>Urabe, Akio</creatorcontrib><creatorcontrib>Takaku, Fumimaro</creatorcontrib><collection>Istex</collection><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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kitamura, Toshio</au><au>Tange, Tsuyoshi</au><au>Terasawa, Takashi</au><au>Chiba, Shigeru</au><au>Kuwaki, Tomoaki</au><au>Miyagawa, Kiyoshi</au><au>Piao, Yun-Feng</au><au>Miyazono, Kohei</au><au>Urabe, Akio</au><au>Takaku, Fumimaro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Establishment and characterization of a unique human cell line that proliferates dependently on GM-CSF, IL-3, or erythropoietin</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J. Cell. Physiol</addtitle><date>1989-08</date><risdate>1989</risdate><volume>140</volume><issue>2</issue><spage>323</spage><epage>334</epage><pages>323-334</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><coden>JCLLAX</coden><abstract>We have established a novel cell line, designated as TF‐1, from a patient with erythroleukemia, which showed complete growth dependency on granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) or on interleukin‐3 (IL‐3) and carried a homogeneous chromosomal abnormality (54X). Erythropoietin (EPO) also sustained the short‐term growth of TF‐1, but did not induce erythroid differentiation. These three hematopoietic growth factors acted on TF‐1 synergistically. Transforming growth factorβ and interferons inhibited the factor‐dependent growth of TF‐1 cells in a dose‐dependent fashion, and monocyte‐colony stimulating factor and interkeukin‐1 enhanced the GM‐CSF‐dependent growth of TF‐1. Ultrastructural studies revealed some very immature features in this cell line. Although TF‐1 cells do not express glycophorin A or carbonyl anhydrase I, the morphological and cytochemical features, and the constitutive expression of globin genes, indicate the commitment of TF‐1 to erythroid lineage. When induced to differentiate, TF‐1 entered two different pathways. Specifically, hemin and delta‐arninolevulinic acid induced hemoglobin synthesis, whereas TPA induced dramatic differentiation of TF‐1 into macrophage‐like cells. In summary, TF‐1 is a cell lineof immature erythroid origin that requires GM‐CSF, IL‐3, or EPO for its growth and that has the ability to undergo differentiation into either more mature erythroid cells or into macrophage‐like cells. TF‐1 is auseful tool for analyzing the human receptors for IL‐3, GM‐CSF, and EPO or the signal transduction of these hemopoietic growth factors.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>2663885</pmid><doi>10.1002/jcp.1041400219</doi><tpages>12</tpages></addata></record>
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subjects Adult
Animal cells
Antigens, Surface - analysis
Biological and medical sciences
Bone Marrow - analysis
Bone Marrow - drug effects
Bone Marrow - pathology
Cell cultures. Hybridization. Fusion
Cell Line
Cell Transformation, Neoplastic - drug effects
Colony-Stimulating Factors - pharmacology
Erythropoietin - pharmacology
Fundamental and applied biological sciences. Psychology
Granulocyte-Macrophage Colony-Stimulating Factor
Growth Substances - pharmacology
Humans
Interleukin-3 - pharmacology
Leukemia, Erythroblastic, Acute - pathology
Male
Mitosis
Molecular and cellular biology
Stem Cells - pathology
Tumor Cells, Cultured - analysis
Tumor Cells, Cultured - pathology
title Establishment and characterization of a unique human cell line that proliferates dependently on GM-CSF, IL-3, or erythropoietin
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