Differentiation of a human eosinophilic leukemic cell line, EoL-1: characterization by the expression of cytokine receptors, adhesion molecules, CD95 and eosinophilic cationic protein (ECP)

Wong, Chun‐Kwok; Ho, C. Y.; Lam, Ching Wan; Zhang, J.P; Hjelm, N M

doi:10.1016/s0165-2478(99)00064-4

Cited by 26 publications

(24 citation statements)

References 32 publications

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“…1D). Our results agree with previous studies, showing that EoL-1 cells under normal culture conditions express a high level of CD49d and very little CD11b and that the expression of CD49d decreases and CD11b increases under differentiating stimuli (16,28). On the other hand, ATRA had no effect on CD14 and intracellular or extracellular IL5Ra expression.…”

Section: Resultssupporting

confidence: 92%

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Apoptosis Induction by Retinoids in Eosinophilic Leukemia Cells: Implication of Retinoic Acid Receptor-α Signaling in All-Trans-Retinoic Acid Hypersensitivity

et al. 2006

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Hypereosinophilic syndrome (HES) has recently been recognized as a clonal leukemic lesion, which is due to a specific oncogenic event that generates hyperactive platelet-derived growth factor receptor-A-derived tyrosine kinase fusion proteins. In the present work, the effect of retinoids on the leukemic hypereosinophilia-derived EoL-1 cell line and on primary HES-derived cells has been investigated. We show that all-trans-retinoic acid (ATRA) inhibits eosinophil colony formation of HES-derived bone marrow cells and is a powerful inducer of apoptosis of the EoL-1 cell line. Apoptosis was shown in the nanomolar concentration range by phosphatidylserine externalization, proapoptotic shift of the Bcl-2/Bak ratio, drop in mitochondrial membrane potential, activation of caspases, and cellular morphology. Unlike in other ATRAsensitive myeloid leukemia models, apoptosis was rapid and was not preceded by terminal cell differentiation. Use of isoform-selective synthetic retinoids indicated that retinoic acid receptor-A-dependent signaling is sufficient to induce apoptosis of EoL-1 cells. Our work shows that the scope of ATRA-induced apoptosis of malignancies may be wider within the myeloid lineage than thought previously, that the EoL-1 cell line constitutes a new and unique model for the study of ATRA-induced cell death, and that ATRA may have potential for the management of clonal HES. (Cancer Res 2006; 66(12): 6336-44)

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Section: Resultssupporting

confidence: 92%

“…The EoL-1 cell line constitutes the only in vitro tool currently available for the study of this type of malignancy and has recently been used by many laboratories for the investigation of eosinophil-granulocytic differentiation (13,16,17) and the function of the FIP1L1/PDGFR-a fusion protein (5,15,18).…”

Section: Introductionmentioning

confidence: 99%

Apoptosis Induction by Retinoids in Eosinophilic Leukemia Cells: Implication of Retinoic Acid Receptor-α Signaling in All-Trans-Retinoic Acid Hypersensitivity

et al. 2006

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“…We also evaluated the effect of anti-EGFL7 treatment on differentiation of AML cells by measuring CD11b expression. CD11b is a surface marker reported to be up-regulated upon differentiation of leukemic cell lines into macrophage-like cells (17,18). We found that EGFL7 inhibition led to significant increases in CD11b expression in all four cell lines that were treated with the anti-EGFL7 antibody compared with treatment with human IgG control (Fig.…”

Section: Differential Effect Of Egfl7 Silencing On Aml Blasts and Normalmentioning

confidence: 99%

Prognostic and biological significance of the proangiogenic factor EGFL7 in acute myeloid leukemia

Papaioannou

Shen

Nicolet

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Epithelial growth factor-like 7 (EGFL7) is a protein that is secreted by endothelial cells and plays an important role in angiogenesis. Although EGFL7 is aberrantly overexpressed in solid tumors, its role in leukemia has not been evaluated. Here, we report that levels of both EGFL7 mRNA and EGFL7 protein are increased in blasts of patients with acute myeloid leukemia (AML) compared with normal bone marrow cells. High EGFL7 mRNA expression associates with lower complete remission rates, and shorter event-free and overall survival in older (age ≥60 y) and younger (age <60 y) patients with cytogenetically normal AML. We further show that AML blasts secrete EGFL7 protein and that higher levels of EGFL7 protein are found in the sera from AML patients than in sera from healthy controls. Treatment of patient AML blasts with recombinant EGFL7 in vitro leads to increases in leukemic blast cell growth and levels of phosphorylated AKT. EGFL7 blockade with an anti-EGFL7 antibody reduced the growth potential and viability of AML cells. Our findings demonstrate that increased EGFL7 expression and secretion is an autocrine mechanism supporting growth of leukemic blasts in patients with AML. EGFL7 | acute myeloid leukemia | clinical outcomeA cute myeloid leukemia (AML) is a clonal hematopoietic disease characterized by the proliferation of immature blasts in the bone marrow (BM) and blood (1). Genetic alterations, including chromosomal translocations and deletions and gene mutations leading to aberrant downstream target gene expression, contribute to AML initiation and maintenance. Previously, our group demonstrated that increased miRNA-126-3p (miR-126) expression in patients with cytogenetically normal AML (CN-AML) correlated with shorter overall survival (OS). Furthermore, we found miR-126 to be essential for leukemia stem cell (LSC) homeostasis, and in vivo targeting of miR-126 in a patientderived xenograft model resulted in prolonged survival in secondary bone marrow transplant (BMT) recipients (2). miR-126 is located within intron 7 of a protein-coding gene known as Epithelial growth factor-like 7 (EGFL7) (3). Although we and others (2, 4, 5) have shown an important role for miR-126 in AML biology, we know of no studies that have been performed to understand the prognostic and functional implications of expression of its host gene, EGFL7, in AML.EGFL7 is a secreted protein of ∼30 kDa and plays an important physiological role in angiogenesis (6-8). Unlike other angiogenic factors (e.g., VEGF), physiological EGFL7 expression and function has been restricted mainly to the endothelial cells where it regulates survival, migration, and differentiation (6). Aberrant expression of EGFL7 has been shown to be involved in tumor growth and disease progression of several solid tumors, including hepatocellular carcinoma, malignant glioma, and breast, lung, and pancreatic cancers (9), but its role in hematopoietic malignancies is currently unknown. Therefore, we investigated the prognostic and biological function of EGFL7 expression in A...

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“…EOL-1 cells are known to respond to phorbol myristate acetate ester (PMA) treatment and they provide a useful experimental model for the study of differentiation and regulation of human eosinophils. Moreover, EOL-1 cells are suitable as an in vitro eosinophilic model for studying eosinophilic functions [31,32]. Taking into account these considerations, PMA differentiated human EOL-1 cells were applied in a co-cultural model with HT-29 cells untreated or pretreated with pure budesonide or budesonide loaded nanoparticles.…”

Section: Cytoprotective Effectmentioning

confidence: 99%

Functionalized mesoporous silica nanoparticles for oral delivery of budesonide

Yoncheva

Popova

Szegedi

et al. 2014

Journal of Solid State Chemistry

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A b s t r a c tNon-functionalized and amino-functionalized mesoporous silica nanoparticle were loaded with anti-inflammatory drug budesonide and additionally post-coated with bioadhesive polymer (carbopol). TEM images showed spherical shape of the nanoparticles and slightly higher polydispersity after coating with carbopol. Nitrogen physisorption and thermogravimetic analysis revealed that more efficient loading and incorporation into the pores of nanoparticles was achieved with the amino-functionalized silica carrier. Infrared spectra indicated that the post-coating of these nanoparticles with carbopol led to the formation of bond between amino groups of the functionalized carrier and carboxyl groups of carbopol. The combination of amino-functionalization of the carrier with the post-coating of the nanoparticles sustained budesonide release. Further, an in vitro model of inflammatory bowel disease showed that the cytoprotective effect of budesonide loaded in the post-coated silica nanoparticles on damaged HT-29 cells was more pronounced compared to the cytoprotection obtained with pure budesonide.

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Differentiation of a human eosinophilic leukemic cell line, EoL-1: characterization by the expression of cytokine receptors, adhesion molecules, CD95 and eosinophilic cationic protein (ECP)

Cited by 26 publications

References 32 publications

Apoptosis Induction by Retinoids in Eosinophilic Leukemia Cells: Implication of Retinoic Acid Receptor-α Signaling in All-Trans-Retinoic Acid Hypersensitivity

Apoptosis Induction by Retinoids in Eosinophilic Leukemia Cells: Implication of Retinoic Acid Receptor-α Signaling in All-Trans-Retinoic Acid Hypersensitivity

Prognostic and biological significance of the proangiogenic factor EGFL7 in acute myeloid leukemia

Functionalized mesoporous silica nanoparticles for oral delivery of budesonide

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