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DLK1 affects T cell acute lymphoblastic leukemia cells by regulating Notch pathway / 白血病·淋巴瘤
Journal of Leukemia & Lymphoma ; (12): 586-588, 2013.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-466634
Biblioteca responsável: WPRO
ABSTRACT
Objective To detect the proliferation and the expression levels of downstream target genes of Notch pathway of T-ALL CCRF-CEM(CEM)cell line treated with exogenous DLK1 protein,in order to investigatethe effects of DLK1 protein on the Notch pathway in CEM cells.Methods CCK-8 assay was performed to examine the proliferation of CCRF-CEM cells,which were treated with various concentration(0.5,1.0,1.5 μg/ml)DLK1 for various time(24,48,72 h).RFQ-PCR was applied to assess the mRNA expression level of Notch1 receptor and downstream target genes of Notch pathway in CEM cells,which were treated for various time(24,48,72 h).Results DLK1 protein stimulated the proliferation of CCRF-CEM cells,and the proliferation rates with different concentrations of DLK1 were 0.14±0.03,0.17±0.04,0.55±0.01 in 72 hours,respectively,there were statistic differences between that in the experimental group and that in the control group(P<0.05).DLK1 protein up-regulated the Notch1 receptor and its downstream target genes HES1,c-myc and NF-κB.The relative transcript levels of target genes HES1 in 72 hours,c-myc in 48 hours and NF-κB in 72 hours were 3.2551±0.3100,1.6086±0.0941,2.0515±0.3453 respectively,and there were statistic differences between that in the experimental group and that in the control group(P<0.05).Conclusion DLK1 protein stimulates the proliferation of T-ALL CCRF-CEM cells by up-regulating Notch1 receptor and downstream target genes HES1,c-myc and NF-κB of Notch pathway.

Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of Leukemia & Lymphoma Ano de publicação: 2013 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of Leukemia & Lymphoma Ano de publicação: 2013 Tipo de documento: Artigo
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