Regulation of all-trans retinoic acid and arsenic trioxide on CD44v6 expression in NB4 cells / 中国实验血液学杂志
Journal of Experimental Hematology
;
(6): 33-37, 2012.
Artículo
en Chino
| WPRIM
| ID: wpr-331027
ABSTRACT
The adhesion molecule CD44 variant isoform (CD44v6) closely associates with progress of acute myeloid leukemia (AML). This study was purposed to investigate the effects of all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) on the expression of CD44v6 and the associated signal pathway phosphatidylinositol 3-kinase (PI3K)/Akt in acute promyelocytic leukemia (APL) cell line NB4 cells. The differentiation of NB4 was detected by morphologic observation and flow cytometry; the NB4 cell apoptosis was assayed by flow cytometry with Annexin V-FITC/PI double staining; the CD44v6 mRNA expression in NB4 cells was determined by real-time RT-PCR, the CD44v6 protein expression and changes of PI3K/Akt signal pathway in NB4 cells were analysed by Western blot. The results demonstrated that in ATRA-induced differentiation, the transcriptional level of CD44v6 was dominantly down-regulated, the translational level of CD44v6 did not change and the PI3K/Akt signal axis was activated. In As2O3-induced apoptosis, both the transcriptional level and translational level of CD44v6 were remarkably reduced, and the PI3K/Akt pathway was inhibited. It is concluded that the regulation of ATRA on expression of CD44v6 in NB4 cells differs from that of As2O3. The results provide an experimental basis to reveal the different mechanism of ATRA and As2O3 in view of the intercommunication between leukemia cells and hematopoietic microenvironment.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Óxidos
/
Patología
/
Farmacología
/
Arsenicales
/
Tretinoina
/
Leucemia Promielocítica Aguda
/
Transducción de Señal
/
Regulación Leucémica de la Expresión Génica
/
Diferenciación Celular
/
Receptores de Hialuranos
Límite:
Humanos
Idioma:
Chino
Revista:
Journal of Experimental Hematology
Año:
2012
Tipo del documento:
Artículo
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