The study on the mechanism of CRKL gene involved in K562/ADM
10.3760/cma.j.issn.0254-9026.2009.11.023
- VernacularTitle:CT10调节子样激酶对人白血病耐阿霉素细胞株细胞耐药作用机制的研究
- Author:
Huanxing LIU
;
Shaohua SHEN
;
Chunhua QI
;
Xianyong YANG
- Publication Type:Journal Article
- Keywords:
Leukemia;
Multidrug resistance-associated proteins;
Signal transduction
- From:
Chinese Journal of Geriatrics
2009;28(11):946-949
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the mechanism and way for CT10 regulator of kinase like (CRKL) involving in drug resistance in leukemia cells. Methods The four major proteins included Ras protein, signal transducer and activator of transcripton 5 (STAT5) protein, phosphoinositide 3-kinase (PI3K) protein and paxillin protein in leukemia which involved in signal transduction pathway of CRKL. The expressions of those proteins were detected by Western-blot and immunofluorescent staining and confocal laser scanning microscopy. Results Compared with K562/S cells, the expressions of Ras(41.52±15.47 vs. 23.74±8.67) and PI3K (35.60±12.48 vs. 10.09±0.005) protein were up-regulated in K562/ADM cells (t=3.01,6.13;both P<0.05), while there were no significant changes in the expressions of paxillin (20.10±11.89 vs. 23.11±12.40) and STAT5 protein (25.72±14.46 vs. 17.58±9.21) between K562/S cells and K562/ADM cells(t=0. 18,1.43;both P>0. 0S). Conclusions Ras and PI3K protein may play a role in the multidrug resistance of K562 cell line, while paxillin and STAT5 protein may be not involved in the formation of resistant in K562 cells.
