Influence of BCR-ABL inhibitor STI571 on SARI expression in K562 cells.
- Author:
Qing HUANG
1
;
Xiao-Qing LI
;
Yan YANG
;
Shi-Ang HUANG
Author Information
1. Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
- Publication Type:Journal Article
- MeSH:
Basic-Leucine Zipper Transcription Factors;
genetics;
Benzamides;
Fusion Proteins, bcr-abl;
antagonists & inhibitors;
Gene Expression Regulation, Leukemic;
drug effects;
Humans;
Imatinib Mesylate;
K562 Cells;
Piperazines;
pharmacology;
Pyrimidines;
pharmacology;
Tumor Suppressor Proteins;
genetics
- From:
Journal of Experimental Hematology
2011;19(4):865-868
- CountryChina
- Language:Chinese
-
Abstract:
In order to investigate the molecular mechanisms of SARI expression regulation in chronic myeloid leukemia (CML), 46 patients with CML and 40 healthy volunteers were recruited in this study. SARI expression in the peripheral blood mononuclear cells (PBMNC) of CML patients and healthy volunteers was assayed by using real-time quantitative PCR. K562 cells were in vitro incubated with the BCR-ABL inhibitor STI571 (imatinib) at 37°C and 5% CO2 for 24 hours, then SARI expression was detected by using real-time quantitative PCR. All experiments were repeated three times. The results showed that as compared with healthy volunteers, the expression of SARI mRNA in PBMNC of CML patients presented a lower level (p < 0.001). After exposure of K562 cells to STI571 (2.5 µmol/L) for 24 hours, the SARI expression was higher than that in K562 cells treated without STI571 (p < 0.001). It is concluded that the suppression of SARI expression is involved in CML pathogenesis, and BCR-ABL mediates the down-regulation of SARI mRNA expression in K562 cells. These findings suggest a new orientation for gene therapy in CML patients.
