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Effect of microRNA-17-92 cluster on the biological characteristics of K562 cells and its mechanisms / 中国实验血液学杂志
Journal of Experimental Hematology ; (6): 20-24, 2014.
Artículo en Chino | WPRIM | ID: wpr-264957
ABSTRACT
The objective of this study was to explore the effects of microRNA-17-92 on the biological characteristics of K562 cells. The expression of miR-17-92 in K562 cells transfected with miRNA-17-92 mimic was detected by real time PCR. The effect of microRNA-17-92 on K562 cell proliferation was detected by CCK-8 method. Apoptosis of K562 cells was detected by Annexin V-PI labeling. Cell cycle distribution was determined by using flow cytometry. Western blot was performed to determine the protein levels of Crk. The results indicated that the transfection with miR-17-92 mimic increased expression of mature miR-17-92 in K562 cells. Compared with control group, cell proliferation and cell amount in S-phase of miR-17-92 mimic transfected group significantly increased, cell apoptosis decreased. The expression of signal connector protein Crk was greatly up-regulated in miR-17-92-mimic-transfected K562 cells. It is concluded that miR-17-92 can promote proliferation, inhibit apoptosis and regulate the cell cycle of K562 cells.
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Transfección / Leucemia Mielógena Crónica BCR-ABL Positiva / Regulación Leucémica de la Expresión Génica / Ciclo Celular / Apoptosis / Células HL-60 / Células K562 / MicroARNs / Proliferación Celular / Genética Límite: Humanos Idioma: Chino Revista: Journal of Experimental Hematology Año: 2014 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Transfección / Leucemia Mielógena Crónica BCR-ABL Positiva / Regulación Leucémica de la Expresión Génica / Ciclo Celular / Apoptosis / Células HL-60 / Células K562 / MicroARNs / Proliferación Celular / Genética Límite: Humanos Idioma: Chino Revista: Journal of Experimental Hematology Año: 2014 Tipo del documento: Artículo