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Journal of Experimental Hematology ; (6): 1157-1161, 2013.
Article in Chinese | WPRIM | ID: wpr-283962


The purpose of this study was to investigate the effects of Celecoxib on the proliferation of the FLT3-ITD positive and negative acute myeloid leukemia cells and its mechanism. The proliferation inhibition effect of Celecoxib with different doses on the FLT3-ITD positive cells MV4-11 and the FLT3-ITD negative K562 cells was detected by CCK-8 method, the cell apoptosis was determined by flow cytometry, and the MEK, Mcl-1, pAKT expression was tested by Western blot. The results showed that Celecoxib inhibited the proliferation of both MV4-11 and K562 cells, but the IC50 for MV4-11 was (29.14 ± 2.4) µmol/L, which was significantly lower than that of K562 cells (39.84 ± 1.0) µmol/L (P < 0.05); The induced apoptosis rate of Celecoxib at 20-80 µmol/L on MV4-11 was not observed, but there was apparent influence on K562 at the same concentration. Western blot showed that Celecoxib down-regulated the expression of MEK and Mcl-1 but did not change the expression of pAKT obviously on MV4-11 cells, while the expression of Mcl-1 was reduced a little, but no obvious change were found in the expression of MEK and pAKT on K562 cells. It is concluded that the Celecoxib can inhibit the proliferation of FLT3-ITD positive AML cells distinctly, and the potential mechanism may be related to the inhibition of the MEK/Mcl-1 signaling pathway.

Humans , Apoptosis , Celecoxib , Cell Proliferation , Cyclooxygenase 2 Inhibitors , Pharmacology , Gene Expression Regulation, Leukemic , K562 Cells , Leukemia, Myeloid, Acute , Drug Therapy , Metabolism , Pathology , MAP Kinase Kinase 1 , Genetics , Myeloid Cell Leukemia Sequence 1 Protein , Genetics , Proto-Oncogene Proteins c-akt , Genetics , Pyrazoles , Pharmacology , Signal Transduction , Sulfonamides , Pharmacology , fms-Like Tyrosine Kinase 3 , Genetics