Methylation of CHD5 Gene Promoter Regulates p19/p53/p21 Pathway to Facilitate Pathogenesis of Acute Myeloid Leukemia / 中国实验血液学杂志
Journal of Experimental Hematology
; (6): 1001-1007, 2019.
Article
em Zh
| WPRIM
| ID: wpr-771848
Biblioteca responsável:
WPRO
ABSTRACT
OBJECTIVE@#To investigate the methylation status of CHD5 gene promoter in bone marrow from acute myeloid leukemia (AML) patients, and the underlying mechanism for initiating the pathogenesis of AML via p19/p53/p21 pathway.@*METHODS@#Methylation status of the CHD5 gene promoter was detected by using methylation-specific polymerase chain reaction (MSPCR) in bone marrow from AML patients, and the iron-deficiency anemia (IDA) samples were served as control. The expression of CHD5, p19, p53 and p21 was determined by real-time quantitative reverse transcriptase PCR and Western blot.@*RESULTS@#The methylation of CHD5 gene in bone marrow from AML patients increased significantly (39.06%) as compared with control group (6.67%). The methylation of CHD5 gene significantly correlated with chromosome karyotype differentiation (P<0.01), but did not correlate with the patient's sex, age and clinical classification (P>0.05). The mRNA expression of CHD5 gene in AML decreased, compared with control group, the mRNA and protein expression of p19, p53 and p21 in AML with CHD5 methylation promoter decreased.@*CONCLUSION@#The hypermeltylation of CHD5 gene promoter in AML patients can lead to decrease of CHD5, p19, p53 and p21 expression levels which may reduce the inhibitory effect on proliferation of leukemia cells through the regulation of p19, p53 and p21 pathway, thus promotes the occurence of AML.
Texto completo:
1
Base de dados:
WPRIM
Assunto principal:
Leucemia Mieloide Aguda
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Proteína Supressora de Tumor p53
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Regiões Promotoras Genéticas
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DNA Helicases
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Metilação de DNA
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Inibidor p16 de Quinase Dependente de Ciclina
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Inibidor de Quinase Dependente de Ciclina p21
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Proteínas do Tecido Nervoso
Tipo de estudo:
Etiology_studies
Limite:
Humans
Idioma:
Zh
Ano de publicação:
2019
Tipo de documento:
Article