Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
Adicionar filtros








Intervalo de ano
1.
Journal of Experimental Hematology ; (6): 76-80, 2023.
Artigo em Chinês | WPRIM | ID: wpr-971105

RESUMO

OBJECTIVE@#To investigate the effects of miR-144-3p on cell proliferation, cell cycle and apoptosis of blast phase chronic myelogenous leukemia (CML) K562 cells.@*METHODS@#K562 cells were cultured in vitro and mimics negative control, hsa-miR-144-3p mimics, inhibitor negative control and miR-144-3p inhibitor were respectively transfected into K562 cells with transfection reagents. The cells were divided into five groups including blank control, mimics negative control, miR-144-3p mimics, inhibitor negative control and miR-144-3p inhibitor. After transfection, the cell proliferation activity was detected by CCK-8 assay. The cell cycle distribution and apoptosis were detected by flow cytometry.@*RESULTS@#Compared with the blank control and mimics negative control groups, the proliferation rate of miR-144-3p mimics group was significantly decreased (P<0.05), the proportion of S phase cells was markedly increased (P<0.05), while the proportion of G1 phase cells was obviously decreased (P<0.05), and the apoptosis rate was significantly increased (P<0.05). Compared with the blank control and inhibitor negative control groups, the proliferation rate of miR-144-3p inhibitor group was obviously increased (P<0.05), the proportion of S phase cells was markedly decreased (P<0.05), while the proportion of G1 phase cells was obviously increased (P<0.05), and the apoptosis rate was significantly decreased (P<0.05).@*CONCLUSION@#miR-144-3p can inhibit the proliferation and promote apoptosis of K562 cells, affect the cell cycle, and block K562 cells in S phase, which indicates that miR-144-3p is involved in the cell cycle activity of CML during blastic phase.


Assuntos
Humanos , Apoptose/genética , Ciclo Celular/genética , Linhagem Celular Tumoral , Proliferação de Células/genética , Células K562 , MicroRNAs/metabolismo
2.
Journal of Experimental Hematology ; (6): 1477-1481, 2017.
Artigo em Chinês | WPRIM | ID: wpr-301703

RESUMO

<p><b>OBJECTIVE</b>To investigate the clinical efficacy of decitabine combined with low-dose IA for treating patients with myelodysplastic syndrome-EB.</p><p><b>METHODS</b>Thirty-seven cases of myelodysplastic syndrome-EB patients diagnosed in the First Affiliated Hospital of Xi'an Jiaotong University from June 2015 to January 2017 were analyzed retrospectively. These patients accepted DAC+IA(19 cases) and DAC(18 cases) treatment separately, and the differences of clinical efficacy between them were compared.</p><p><b>RESULTS</b>After 1-2 treatment cycles, in DAC+IA group the rate of complete remission with full hematologic recovery and incomplete hematologic recovery was 57.9%, and overall response rate was 100%. Immature cells level observed in bone marrow pathology was significantly decreased, compared with level before treatment. Peripheral blood neutrophil count, hemoglobin level and platelet count increased significantly. The median duration of the complete remission was 7.3 months. The progression free survival time was 10 months. Three patients with complete remission relapsed after interruption of treatment for 3.5 months. In DAC group complete remission rate was 16.7%, and overall response rate was 38.9%. The progression free survival lasted for 6 months. The median time of 3 complete remission patients transformed to AML was 4 months. The common adverse reactions were myelosuppression and infection without significant difference between the 2 groups.</p><p><b>CONCLUSION</b>The regimen of decitabine combinated with low-dose IA for treating patients with myelodysplastic syndrome-EB is effective, which can prolong the survival and improve the quality of life, whereas the long-term effect needs to be consolidated by allogeneic hematopoietic stem cell transplantation.</p>

3.
Journal of Experimental Hematology ; (6): 492-497, 2016.
Artigo em Chinês | WPRIM | ID: wpr-360060

RESUMO

<p><b>OBJECTIVE</b>To explore the autophagy of RPMI8226 cells induced by As(2)O(3) and its possible mechanisms.</p><p><b>METHODS</b>RPMI8226 was incubated with different concentration of As(2)O(3) for different time, and the inhibiting rate was calculated by MTT method. The autophagic rate of RPMI8226 cells incubated with different concentration of As(2)O(3) was determined by FACS. The change of cells ultrastructure was observed by transmission electron microsopy (TEM). After incubation with different concentration of As(2)O(3), the expression of Beclin-1 on RPMI8226 was detected by RT-PCR and Western blot.</p><p><b>RESULTS</b>Different concentration of As(2)O(3) could significantly inhibit the proliferation of RPMI8226 cells (P < 0.05), and the inhibitory effect was in dose- and time-dependent way in a certain range. the autophagic rate increased with the increasing of drug concentration and prolonging of action time (P < 0.05). TEM results revealed a typical autophagosome in RPMI-8226 cell treated by As(2)O(3) for 48 hours. Beclin-1 was up-regulated in RPMI 8226 cells when treated with different concentration of As(2)O(3) for 48h (P < 0.05).</p><p><b>CONCLUSION</b>As(2)O(3) can induce autophagy of RPMI8226 cells, and the mechanism may be associated with the upregulation of Beclin-1.</p>


Assuntos
Humanos , Proteínas Reguladoras de Apoptose , Metabolismo , Arsenicais , Farmacologia , Autofagia , Proteína Beclina-1 , Linhagem Celular Tumoral , Proliferação de Células , Proteínas de Membrana , Metabolismo , Óxidos , Farmacologia , Regulação para Cima
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA