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C/EBPα在慢性髓性白血病患者中的表达及其作用机制研究

OBJECTIVE: To investigate the expression and the possible mechanism of the transcription factor C/EBPα in chronic myeloid leukemia (CML). METHODS: Bone marrow samples from 50 CML patients (including 33 patients in chronic phase, 7 in accelerated phase and 10 in blast crisis) and peripheral blood spe...

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Detalles Bibliográficos
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Editorial office of Chinese Journal of Hematology 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7342430/
https://www.ncbi.nlm.nih.gov/pubmed/26632469
http://dx.doi.org/10.3760/cma.j.issn.0253-2727.2015.11.012
Descripción
Sumario:OBJECTIVE: To investigate the expression and the possible mechanism of the transcription factor C/EBPα in chronic myeloid leukemia (CML). METHODS: Bone marrow samples from 50 CML patients (including 33 patients in chronic phase, 7 in accelerated phase and 10 in blast crisis) and peripheral blood specimens of 20 healthy donors were collected. The expression of C/EBPα gene and the effect of Imatinib on its expression was detected by RT-PCR. C/EBPα gene was inserted into lentivirus expression vector pLVX-EGFP-3FLAG-Puro by recombinant DNA technology to construct C/EBPα stable expression in K562 cells. Cell proliferation was assayed by CCK-8. The expressions of Foxo3a and Bim genes were detected by RT-PCR. RESULTS: The level of C/EBPα expression was significantly declined in CML patients compared with that of normal control group (P<0.01) and had negative correlation with bcr-abl expression (Spearman r= –0.505, P<0.01). The stable K562-C/EBPα cell line was successfully established and confirmed by RT-PCR and Western blot. Cell proliferation ability was lower in the K562-C/EBPα group than that in the non-transfection and mock-vehicle groups. The expressions of Foxo3a and Bim genes were 1.06 ± 0.06 and 0.53 ± 0.07, respectively, which was higher than that of non-transfection and mock-vehicle groups (P<0.01, P<0.05). CONCLUSION: C/EBPα expression was decreased in CML patients, overexpression of C/EBPα could inhibit K562 cell growth.