| Registro completo |
| Provedor de dados: |
Genet. Mol. Biol.
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| País: |
Brazil
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| Título: |
MicroRNA-21 over expression in umbilical cord blood hematopoietic stem progenitor cells by leukemia microvesicles
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| Autores: |
Razmkhah,Farnaz
Soleimani,Masoud
Ghasemi,Sorayya
Kafi-abad,Sedigheh Amini
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| Data: |
2019-06-01
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| Ano: |
2019
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| Palavras-chave: |
Leukemia
Microvesicles
Hematopoietic stem cells
MicroRNA-21
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| Resumo: |
Abstract Microvesicles are able to induce the cell of origin’s phenotype in a target cell. MicroRNA-21, as an oncomir, is up-regulated in almost all cancer types such as leukemia which results in cell proliferation. In this study, we examine the ability of leukemia microvesicles to induce proliferation in hematopoietic stem progenitor cells (HSPCs) via microRNA-21 dysregulation. Herein, leukemia microvesicles were isolated from HL-60 and NB-4 cell lines by ultracentrifugation, and then their protein content was measured. Normal HSPCs were isolated from umbilical cord blood samples by a CD-34 antibody. These cells were treated with 20 and 40 μg/mL leukemia microvesicles for 5 and 10 days, respectively. Cell count, CD-34 analysis, and a microRNA-21 gene expression assay were done at days 5 and 10. HSPCs showed a significant increase in both microRNA-21 gene expression and cell count after treating with leukemia microvesicles compared with the control group. CD-34 analysis as stemness proof did not show any difference among the studied groups. This data suggests that HSPC proliferation followed by microRNA-21 gene over expression can be another evidence of a leukemia-like phenotype induction in a healthy target cell by leukemia microvesicles.
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| Tipo: |
Info:eu-repo/semantics/article
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| Idioma: |
Inglês
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| Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572019000300465
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| Editor: |
Sociedade Brasileira de Genética
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| Relação: |
10.1590/1678-4685-gmb-2018-0073
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| Formato: |
text/html
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| Fonte: |
Genetics and Molecular Biology v.42 n.2 2019
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| Direitos: |
info:eu-repo/semantics/openAccess
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