Effect of different concentrations of bortezomib on the expression of ERK, JNK and P38 in daunorubicin-resistant K562 cells.
- Author:
Bei-Bei FU
1
;
Ying FAN
;
Liang-Chun HAO
;
Ai-Jun LIAO
;
Zhuo-Gang LIU
Author Information
1. Department of Hematology, China Medical University Shengjing Hospital, Shenyang 110022, Liaoning Province, China.
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents;
administration & dosage;
pharmacology;
Boronic Acids;
administration & dosage;
pharmacology;
Bortezomib;
Drug Resistance, Neoplasm;
Humans;
JNK Mitogen-Activated Protein Kinases;
metabolism;
K562 Cells;
Protease Inhibitors;
administration & dosage;
pharmacology;
Pyrazines;
administration & dosage;
pharmacology;
p38 Mitogen-Activated Protein Kinases;
metabolism
- From:
Journal of Experimental Hematology
2011;19(3):671-675
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study was to investigate the effect of proteasome inhibitor bortezomib on the expression of ERK, JNK, and P38 in daunorubicin (DNR)-resistant K562 cells and its mechanism. MTT method was used to determine the drug-resistant K562 cells and the cellular toxicity of bortezomib; Western blot was used to detect the expression of protein ERK, JNK and P38 in K562 cells after treatment with 100 nmol/L DNR alone or combined with 1 nmol/L and 10 nmol/L bortezomib for 36 hours. Flow cytometry assay was used to detect the apoptosis rate in each group cells. The results indicated that the expression of ERK and P38 were significantly suppressed (p < 0.05) and the expression of JNK was significantly enhanced (p < 0.05) in the cells treated by DNR combined with bortezomib. It is concluded that bortezomib can decrease the expressions of protein ERK and P38 and enhance the expression of JNK, the bortezomib reverses the cellular drug-resistance and promote cell apoptosis through MAPK pathway.
