SphK-1/S1P signal pathway in CML cells / 中国实验血液学杂志
Journal of Experimental Hematology
;
(6): 730-733, 2008.
Article
Dans Chinois
| WPRIM
| ID: wpr-267901
ABSTRACT
Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disease of transformed hematopoietic progenitor cells. In order to investigate the role of sphingosine kinase-1 (SphK-1)/sphingosine 1-phosphate (S1P) signal pathway in the expression of CML cells, and to explore whether P210(bcr/abl) involved is activating SphK-1/S1P signal pathwey, the expressions of SphK-1 and S1P receptor mRNA in bcr/abl positive K562 cells and bcr/abl positive primary CML cells were detected by RT-PCR, the imatinib mesylate, the specific inhibitor of P210(bcr/abl) was employed to inhibit the P210(bcr/abl) tyrosine kinases of K562 cells and CML primary cells, and then the intracellular SphK-1 activity was assayed. The results indicated that after being cultured with 2.5 micromol/L imatinib mesylate for 0.5, 2, 6, 24 and 48 hours, the intensions of inhibiting SphK-1 activity were 0.007%, 38.9%, 34.6%, 28.1% and 76.1% resepectively. SphK-1 activity in CML cells also was reduced by 2.5 micromol/L imatinib mesylate (16.8% - 41.9% decrease). It is concluded that the CML cells express SphK-1 and different S1P receptor, and P210(bcr/abl) fusion protein in CML cells can activate SphK-1.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Pharmacologie
/
Pipérazines
/
Pyrimidines
/
Sphingosine
/
Benzamides
/
ARN messager
/
Lysophospholipides
/
Leucémie myéloïde chronique BCR-ABL positive
/
Transduction du signal
/
Protéines de fusion bcr-abl
Limites du sujet:
Humains
langue:
Chinois
Texte intégral:
Journal of Experimental Hematology
Année:
2008
Type:
Article
Documents relatifs à ce sujet
MEDLINE
...
LILACS
LIS