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Expression of miR-181a in Acute Myeloid Leukaemia and Its Effect on Cell Proliferation / 中国实验血液学杂志
Journal of Experimental Hematology ; (6): 985-989, 2016.
Artigo em Chinês | WPRIM | ID: wpr-246830
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression of miR-181a in AML cell lines and explore its effect on cell proliferation.</p><p><b>METHODS</b>The expression of miR-181a in AML cell lines (NB4,HL-60,K562 and MV-4-11) was detected by quantiative polymerase chain reation(qPCR). Moreover, the cell proliferation and cell cycle were evaluated in several cell lines (HL60, NB4 and K562) by using CCK-8 and flow cytometry after the imitative transfection with miR-181a.</p><p><b>RESULTS</b>The miR-181a expression was significantly increased in most AML cell lines, including NB4,HL-60 and MV-4-11, but decreased in a few AML cell lines(K562), as compared with that in control(P<0.05). Overexpressed miR-181a in the cell lines significantly enhanced the cell proliferation, as well as the cell ratio of S-to and G2-phase by miR-181a imitative transfection in vitro.</p><p><b>CONCLUSION</b>Overexpression of miR-181a can promote AML cell proliferation. MiR-181a may play an oncogene role in AML, studying the MiR-181a may provide a new method for treatment of AML.</p>
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Leucemia Mieloide Aguda / Regulação Neoplásica da Expressão Gênica / Ciclo Celular / MicroRNAs / Linhagem Celular Tumoral / Proliferação de Células / Reação em Cadeia da Polimerase em Tempo Real Limite: Humanos Idioma: Chinês Revista: Journal of Experimental Hematology Ano de publicação: 2016 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Leucemia Mieloide Aguda / Regulação Neoplásica da Expressão Gênica / Ciclo Celular / MicroRNAs / Linhagem Celular Tumoral / Proliferação de Células / Reação em Cadeia da Polimerase em Tempo Real Limite: Humanos Idioma: Chinês Revista: Journal of Experimental Hematology Ano de publicação: 2016 Tipo de documento: Artigo