Comparative proteomic analysis of differentially expressed proteins between K562 and K562/ADM cells

Background Multidrug resistance to chemotherapeutic agents is an important clinical problem during the treatment of leukemia. The resistance process is multifactorial. To realize the total factors involved in multidrug resistance, we analyzed the differentially expressed proteins of K562 and K562/AD...

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Published in:Chinese medical journal 2008-03, Vol.121 (5), p.463-468
Main Authors: Shen, Shao-hua, Gu, Long-jun, Liu, Pei-qing, Ye, Xin, Chang, Wei-shan, Li, Ben-shang
Format: Article
Language:English
Subjects:
Adaptor Proteins, Signal Transducing - analysis
Adaptor Proteins, Signal Transducing - antagonists & inhibitors
Adaptor Proteins, Signal Transducing - genetics
Amino Acid Sequence
Doxorubicin - pharmacology
Drug Resistance, Multiple
Humans
K562 Cells - chemistry
K562 Cells - drug effects
Molecular Sequence Data
Neoplasm Proteins - analysis
Nuclear Proteins - analysis
Nuclear Proteins - antagonists & inhibitors
Nuclear Proteins - genetics
Proteomics
Stathmin - analysis
白血病
药物过敏
蛋白质
阿霉素
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Summary:Background Multidrug resistance to chemotherapeutic agents is an important clinical problem during the treatment of leukemia. The resistance process is multifactorial. To realize the total factors involved in multidrug resistance, we analyzed the differentially expressed proteins of K562 and K562/ADM cells and we investigated one of the up-regulated proteins （CRKL） using siRNA to determine its role in K562/ADM cells. Methods Altered protein expressions between K562/S （K562 ADM-sensitive cell line） and K562/ADM （K562 multidrug resistant cell line induced by adriamycin） were identified by 2D-DIGE coupled with mass spectrometry. Meanwhile, we confirmed the differential expression of CRKL and Stathmin in both K562 and K562/ADM cells by Western blot analysis. Furthermore, we used RNA interference to silence the CRKL gene expression. Results Among the 9 differentially expressed proteins, 3 were up-regulated in K562/ADM cells, while 6 were down-regulated in the K562/ADM cells compared with its parent cell line. The expression of CRKL was up-regulated significantly in K562/ADM cells, and it can be decreased by recombinant lentivirus. Moreover, the multidrug resistance of K562/ADM cells was efficiently reversed by silence of CRKL gene expression. Conclusions The data provided the differentially expressed proteins in K562 and its resistant cell line and highlights the power of 2D-DIGE for the discovery of resistance markers in cancer. We found CRKL may be a new protein involved in the multidrug resistanse of leukaemia cells.
ISSN:0366-6999
2542-5641
DOI:10.1097/00029330-200803010-00019