Reversion of Multidrug-Resistance by Proteasome Inhibitor Bortezomib in K562/DNR Cell Line | |
Alternative Title | Reversion of Multidrug-Resistance by Proteasome Inhibitor Bortezomib in K562/DNR Cell Line |
Wang Huihan; Li Yingchun; Liao Aijun; Fu Beibei; Yang Wei; Liu Zhuogang; Wang Xiaobin | |
2011 | |
Source Publication | CHINESE JOURNAL OF CANCER RESEARCH
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ISSN | 1000-9604 |
Volume | 23Issue:1Pages:69-73 |
Abstract | Objective: To observe the reversion of multi-drug resistance by proteasome inhibitor bortezomib in K562/DNR cell line and to analyze the possible mechanism of reversion of multidrug-resistance. |
Other Abstract | Objective: To observe the reversion of multi‐drug resistance by proteasome inhibitor bortezomib in K562/DNR cell line and to analyze the possible mechanism of reversion of multidrug‐resistance. Methods: MTT method was used to determine the drug resistance of K562/DNR cells and the cellular toxicity of bortezomib. K562/DNR cells were cultured for 12 hours, 24 hours and 36 hours with 100 μg/ml DNR only or plus 4μg/L bortezomib. The expressions of NF‐κB, IκB and P‐gp of K562/DNR were detected with Western blot method, the activity of NF‐κB was tested by ELISA method and the apoptosis rate was observed in each group respectively. Results: The IC50 of DNR on cells of K562/S and K562/DNR groups were 1.16 μg/ml and 50.43 μg/mL, respectively. The drug‐resistant fold was 43.47. The IC10 of PS‐341 on Cell strain K562/DNR was 4 μg/L. Therefore, 4μg/L was selected as the concentration for PS‐341 to reverse drug‐resistance in this study. DNR induced down‐regulation of IκB expression, up‐regulation of NF‐κB and P‐gp expression. After treatment with PS‐341, a proteasome inhibitor, the IκB degradation was inhibited, IκB expression increased, NF‐κB and P‐gp expression decreased in a time dependent manner. Compared to DNR group, the NF‐κB p65 activity of DNR+PS‐341 group was decreased. Compared to Corresponding DNR group, DNR induced apoptosis rate increases after addition of PS‐341 in a time dependent manner. Conclusion: Proteasome inhibitor bortezomib can convert the leukemia cell drug resistance. The mechanism may be that bortezomib decreases the degradation of IκB and the expression of NF‐κB and P‐gp, therefore induces the apoptosis of multi‐drug resistant cells |
Keyword | MULTIPLE-MYELOMA CELLS FACTOR-KAPPA-B CHEMOTHERAPEUTIC-AGENTS THERAPEUTIC TARGET DRUG-RESISTANCE P-GLYCOPROTEIN LEUKEMIA CANCER MALIGNANCIES SENSITIVITY Bortezomib NF-kappa B Multi-drug resistance mdr1 gene P-gp K562 cells |
Indexed By | CSCD |
Language | 英语 |
Funding Project | [Educational Commission of Liaoning Province, China] |
CSCD ID | CSCD:4173900 |
Citation statistics | |
Document Type | 期刊论文 |
Identifier | http://ir.imr.ac.cn/handle/321006/156096 |
Collection | 中国科学院金属研究所 |
Affiliation | 中国科学院金属研究所 |
Recommended Citation GB/T 7714 | Wang Huihan,Li Yingchun,Liao Aijun,et al. Reversion of Multidrug-Resistance by Proteasome Inhibitor Bortezomib in K562/DNR Cell Line[J]. CHINESE JOURNAL OF CANCER RESEARCH,2011,23(1):69-73. |
APA | Wang Huihan.,Li Yingchun.,Liao Aijun.,Fu Beibei.,Yang Wei.,...&Wang Xiaobin.(2011).Reversion of Multidrug-Resistance by Proteasome Inhibitor Bortezomib in K562/DNR Cell Line.CHINESE JOURNAL OF CANCER RESEARCH,23(1),69-73. |
MLA | Wang Huihan,et al."Reversion of Multidrug-Resistance by Proteasome Inhibitor Bortezomib in K562/DNR Cell Line".CHINESE JOURNAL OF CANCER RESEARCH 23.1(2011):69-73. |
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