Resistance and mechanisms underlying the anticancer activity of daunorubicin in CD34+ acute myeloid leukemia cells
- VernacularTitle:CD34+急性髓细胞白血病细胞对柔红霉素耐药机制的初步研究
- Author:
Jia RAO
;
Renwei HUANG
;
Guoan CHEN
;
Rongyan ZHANG
- Publication Type:Journal Article
- Keywords:
acute myeloid leukemia;
daunorubicin;
resistance;
Bcl-2
- From:
Acta Universitatis Medicinalis Anhui
2013;(12):1438-1440
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the resistance and molecular mechanisms underlying the anticancer activity of daunorubicin in CD34 +acute myeloid leukemia(AML) cells. Methods CD34 +AML cell lines(KG1a and Kasu-mi-1)were used as objectives, and CD34 -AML cell line U937 was used as positive control. Western blot analysis was used to examine the protein expression of Bcl-2 and Bax in CD34 +AML and CD34 -AML cell lines incubated with/without daunorubicin to compare the sensitivity of CD34 +AML and CD34 -AML cells to daunorubicin. SiRNA against Bcl-2 was used in KG1a and Kasumi-1 cells and examined the effect on cell viability by MTT assay. Results Western blot analysis showed that Bcl-2 protein levels in CD34 +AML cells appeared to be significantly higher than in CD34 -AML cells. Western blot analysis showed that treatment with 0.4 μg/ml daunorubicin for 48 h caused down-regulation of Bcl-2 only in CD34 -AML cells,but not in CD34 +AML cells. Suppression of Bcl-2 with siRNA increased the susceptibility of KG1a and Kasumi-1 to daunorubicin. Conclusion CD34 +AML cell lines ex-press higher levels of Bcl-2 protein. Daunorubicin fails to down-regulate the high Bcl-2 protein levels in CD34 +AML cells. Suppression of Bcl-2 with siRNA increases the susceptibility of KG1a and Kasumi-1 to daunorubicin. The high Bcl-2 protein levels in CD34 +AML cells may be involved in the insensitivity to daunorubicin.
