CAJ | 학술논문

目的探索CT10调节子样激酶(CRKL)在人白血病细胞中参与耐药的途径及机制.方法应用Western blot检测和免疫荧光染色的激光扫描共聚焦分析技术检测CRKL 4条主要参与白血病发病的传导途径中的相关蛋白,即Ras蛋白、信号转导与转录激活因子5(STAT5)蛋白、磷酸肌醇3激酶(P13K)蛋白以及β1整合素介导的信号转导途径桩蛋白(paxillin蛋白)在白血病敏感细胞株和耐药细胞株中表达的情况. 结果与K562敏感细胞(K562/S)比较,Ras、P13K蛋白在人白血病细胞K562阿霉素耐药细胞株(K562/ADM)中表达增强(41.52±15.47与23.74±8.67、35.60±12.48与10.09±0.01,t=3.01[.13,均P<0.05),而paxillin和sTAT5蛋白在K562/ADM中表达无明显变化(20.10±11.89与23.11±12.40、25.72±14.46与17.58±9.21,t=0.18、1.43,均P>0.05). 结论 CRKL可能通过Ras蛋白和P13K 2条信号转导途径在耐药形成过程中发挥作用,paxillin和STAT5蛋白可能不参与K562细胞耐药的形成.
목적 탐색CT10조절자양격매(CRKL)재인백혈병세포중삼여내약적도경급궤제.방법 응용Western blot검측화면역형광염색적격광소묘공취초분석기술검측CRKL 4조주요삼여백혈병발병적전도도경중적상관단백,즉Ras단백、신호전도여전록격활인자5(STAT5)단백、린산기순3격매(P13K)단백이급β1정합소개도적신호전도도경장단백(paxillin단백)재백혈병민감세포주화내약세포주중표체적정황. 결과여K562민감세포(K562/S)비교,Ras、P13K단백재인백혈병세포K562아매소내약세포주(K562/ADM)중표체증강(41.52±15.47여23.74±8.67、35.60±12.48여10.09±0.01,t=3.01[.13,균P<0.05),이paxillin화sTAT5단백재K562/ADM중표체무명현변화(20.10±11.89여23.11±12.40、25.72±14.46여17.58±9.21,t=0.18、1.43,균P>0.05). 결론 CRKL가능통과Ras단백화P13K 2조신호전도도경재내약형성과정중발휘작용,paxillin화STAT5단백가능불삼여K562세포내약적형성.
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.