Induction of thrombospondin-1 by all-trans retinoic acid modulates growth and differentiation of HL-60 myeloid leukemia cells

Touhami, Myriem; Fauvel-Lafève, Françoise; Silva, N Da; Chomienne, Christine; Legrand, Chantal

doi:10.1038/sj.leu.2400866

Cited by 12 publications

(8 citation statements)

References 23 publications

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“…Beta 1 integrin D U33880 ‫21.5מ‬ 0.0021 1.0000 1.0000 TPO up-regulates adhesion of hematopoetic progenitors to fibronectin through activation of integrin alpha4beta1 and alpha5beta1 (Gotoh et al 1997). Sp4 transcription factor X68561 ‫60.5מ‬ 0.0030 1.0000 1.0000 Sp4 not well characterized but closely related to Sp1 (Suske 1999), TPO activates several Sp1-dependent genes during megakaryopoiesis (Wang et al 1999 (Streit et al 1999), close relative thrombospondin 1 is negative regulator of megakaryopoiesis (Chen et al 1997;Touhami et al 1997 (Marlton et al 1995;Mancini et al 2000), CML/ALL translocations identified in 10q (Kagan et al 1989;Aguiar et al 1997;Salvati et al 1999 (Melnick et al 1999), isochromosomes on 17q common (Fioretos et al 1999) Biglycan J04599 ‫71.4מ‬ 0.2119 1.0000 1.0000 Xq28 Translocation found in AML (Weis et al 1985), common in ALL (Stern 1996 Dataset from Golub et al (1999).…”

Section: Discussionmentioning

confidence: 99%

An Efficient and Robust Statistical Modeling Approach to Discover Differentially Expressed Genes Using Genomic Expression Profiles

Thomas¹,

Olson²,

Tapscott³

et al. 2001

Genome Res.

286

192

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We have developed a statistical regression modeling approach to discover genes that are differentially expressed between two predefined sample groups in DNA microarray experiments. Our model is based on well-defined assumptions, uses rigorous and well-characterized statistical measures, and accounts for the heterogeneity and genomic complexity of the data. In contrast to cluster analysis, which attempts to define groups of genes and/or samples that share common overall expression profiles, our modeling approach uses known sample group membership to focus on expression profiles of individual genes in a sensitive and robust manner. Further, this approach can be used to test statistical hypotheses about gene expression. To demonstrate this methodology, we compared the expression profiles of 11 acute myeloid leukemia (AML) and 27 acute lymphoblastic leukemia (ALL) samples from a previous study ) and found 141 genes differentially expressed between AML and ALL with a 1% significance at the genomic level. Using this modeling approach to compare different sample groups within the AML samples, we identified a group of genes whose expression profiles correlated with that of thrombopoietin and found that genes whose expression associated with AML treatment outcome lie in recurrent chromosomal locations. Our results are compared with those obtained using t-tests or Wilcoxon rank sum statistics.

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Section: Discussionmentioning

confidence: 99%

An Efficient and Robust Statistical Modeling Approach to Discover Differentially Expressed Genes Using Genomic Expression Profiles

Thomas¹,

Olson²,

Tapscott³

et al. 2001

Genome Res.

286

192

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“…Cxcl7 and Cxcl4 block megakaryocyte development, 22 while Cxcl4 also supports the survival and chemosensitivity of hematopoietic cells. 23 Thrombospondin 1 promotes granulocytic 24 and blocks megakaryocyte differentiation. 25 In addition, the cell-cycle inhibitor p16ink4A and the p53 pathway-induced Wig1 gene were both decreased in accordance with the increased cell cycle.…”

Section: Identification Of Genes Altered By Aml1-eto9a In Microarraymentioning

confidence: 99%

The multi-functional cellular adhesion molecule CD44 is regulated by the 8;21 chromosomal translocation

Wang

et al. 2007

Leukemia

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The 8;21 translocation is a common chromosomal abnormality in acute myeloid leukemia (AML). We recently identified a naturally occurring leukemogenic splice variant, AML1-ETO9a (acute myeloid leukemia-1 transcription factor and the eighttwenty-one corepressor-9a), of t(8;21). To understand the leukemic potential of AML1-ETO9a, we performed microarray analysis with the murine multipotential hematopoietic FDCPmix A4 cell line. We identified changes in expression of various genes including CD44. CD44 is a type I transmembrane protein and functions as the major cellular adhesion molecule for hyaluronic acid, a component of the extracellular matrix. CD44 is expressed in most human cell types and is implicated in myeloid leukemia pathogenesis. We show that the presence of AML1-ETO9a significantly increased the expression of CD44 at both RNA and protein levels. Furthermore, the CD44 promoter is bound by AML1-ETO9a and AML1-ETO at the chromatin level. In addition, in the AML1-ETO9a leukemia mouse model CD44 is regulated in a cell context-dependent manner. Thus, our observations suggest that AML1-ETO and its splice variant AML1-ETO9a are able to regulate the expression of the CD44 gene, linking the 8;21 translocation to the regulation of a cell adhesion molecule that is involved in the growth and maintenance of the AML blast/stem cells.

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“…TSP-1 has been described to be positively involved in retinoic acid-induced maturation of neuroblastoma cells and the acute myeloblastic leukemic cell line HL-60. 16,17 In the HL-60 cell line, it was shown to induce a caspase-dependent cell death mediated by CD36. 18 It is also able to trigger a caspase-independent cell death that is accompanied by selective mitochondrial changes in B-chronic lymphocytic leukemia through binding to CD47.…”

Section: Introductionmentioning

confidence: 99%

Type 3 repeat/C-terminal domain of thrombospondin-1 triggers caspase-independent cell death through CD47/αvβ3 in promyelocytic leukemia NB4 cells

Saumet

Slimane

Lanotte

et al. 2005

Blood

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By means of its antiangiogenic activity, thrombospondin-1 (TSP-1) exerts indirect antitumoral action on solid tumors. Here, we investigated potential antitumor action in an in vitro cell model for promyelocytic leukemia (NB4-LR1), resistant to retinoid maturation. Purified soluble TSP-1 added to cultures induced a strong dosedependent growth inhibition and a slowly developing maturation-independent cell death. Recombinant fragments of TSP-1 allowed mapping of these activities to its type 3 repeat/C-terminal domain, features that are distinct from those of TSP-1 action on solid tumors, previously ascribed to the type 1 repeat domain. Cell death in leukemia was characterized as a caspase-independent mechanism, without DNA fragmentation, but phosphatidylserine externalization followed by membrane permeabilization. Mitochondria membrane depolarization was inherent to TSP-1 action but did not produce release of death-promoting proteins (eg, noncaspase apoptosis regulators, apoptosisinduced factor [ IntroductionCell interaction with extracellular matrix proteins is essential to regulate proliferation, differentiation, and cell death. 1-3 Thrombospondin-1 (TSP-1) belongs to a family of multidomain and multifunctional glycoproteins that regulate cell proliferation, migration, and differentiation and is important for embryonic development, morphogenesis, inflammation, tumor metastasis, and multiple other processes. 4-6 TSP-1 is a secreted component of extracellular matrix that supports attachment and motility of a variety of normal and neoplastic cell types. 5,7,8 Because it also functions as soluble protein that antagonizes the proadhesive activities of other matrix proteins, TSP-1 has been defined as a matricellular protein modulating cell-matrix interactions. 9,10 It can affect matrix structure through its ability to interact with matrix components and to activate transforming growth factor-␤1 (TGF-␤1). 11 TSP-1 is also a potent physiological inhibitor of angiogenesis by impairing endothelial cell growth and migration and by acting on endothelial cell cycle progression and apoptosis; thus, down-expression of TSP-1 is important for tumor progression. [12][13][14][15] Many of the TSP-1 functions have been located within specific domains of the molecule that bind to various membrane receptors, including integrins of the ␤1 and ␤3 family, CD47/integrinassociated protein (CD47/IAP), CD36, and proteoglycans. 5,8 Therefore, cell responses to TSP-1 probably reflect the integration of multiple membrane signals depending on the cell type and its repertoire in membrane receptors.TSP-1 function in tumor cell differentiation and apoptosis remains poorly explored. TSP-1 has been described to be positively involved in retinoic acid-induced maturation of neuroblastoma cells and the acute myeloblastic leukemic cell line 17 In the HL-60 cell line, it was shown to induce a caspase-dependent cell death mediated by CD36. 18 It is also able to trigger a caspase-independent cell death that is accompanied by selective mitochondrial changes ...

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Induction of thrombospondin-1 by all-trans retinoic acid modulates growth and differentiation of HL-60 myeloid leukemia cells

Cited by 12 publications

References 23 publications

An Efficient and Robust Statistical Modeling Approach to Discover Differentially Expressed Genes Using Genomic Expression Profiles

An Efficient and Robust Statistical Modeling Approach to Discover Differentially Expressed Genes Using Genomic Expression Profiles

The multi-functional cellular adhesion molecule CD44 is regulated by the 8;21 chromosomal translocation

Type 3 repeat/C-terminal domain of thrombospondin-1 triggers caspase-independent cell death through CD47/αvβ3 in promyelocytic leukemia NB4 cells

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