CAJ | 학술논문

目的探讨蛋白酶体抑制剂硼替佐米对伊马替尼耐药细胞系(K562/G01)药物敏感性的影响及作用机制.方法采用MTT法观察伊马替尼单用与联用硼替佐米对K562/G01细胞增殖的影响.流式细胞技术检测细胞周期的变化.实时荧光定量PCR检测COX-2、多药耐药(mdr1)基因的表达.结果联合10、20 nmol/L硼替佐米能明显增强K562/G01细胞的伊马替尼药物敏感性,逆转倍数分别为1.83、2.72倍,进一步计算表明两药联合具有协同作用.流式细胞技术检测显示硼替佐米作用后细胞周期向G2/M期转化.实时荧光定量PCR检测显示K562/G01细胞高表达的COX-2和mdr1基因,硼替佐米作用后均表达下调.结论硼替佐米能增强K562/G01细胞对伊马替尼的敏感性,其机制可能与细胞周期的G2/M期阻滞,抑制COX-2和mdr1的表达有关.
목적 탐토단백매체억제제붕체좌미대이마체니내약세포계(K562/G01)약물민감성적영향급작용궤제.방법 채용MTT법관찰이마체니단용여련용붕체좌미대K562/G01세포증식적영향.류식세포기술검측세포주기적변화.실시형광정량PCR검측COX-2、다약내약(mdr1)기인적표체.결과 연합10、20 nmol/L붕체좌미능명현증강K562/G01세포적이마체니약물민감성,역전배수분별위1.83、2.72배,진일보계산표명량약연합구유협동작용.류식세포기술검측현시붕체좌미작용후세포주기향G2/M기전화.실시형광정량PCR검측현시K562/G01세포고표체적COX-2화mdr1기인,붕체좌미작용후균표체하조.결론 붕체좌미능증강K562/G01세포대이마체니적민감성,기궤제가능여세포주기적G2/M기조체,억제COX-2화mdr1적표체유관.
Objective To explore the effect of bortezomib ( BOR) on the drug sensitivity of imatinibresistant chronic myeloid leukemia cell line K562/G01 cell and its mechanism. Methods MTT assay was used to detect the inhibition effect of cell growth, flow cytometry to cell cycle, and real time-PCR to the expression of COX-2 and mdrl mRNA. Results Combination of 10 and 20 nmol/L BOR with imatinib could significantly enhance the sensitivity of K562/G01 to imatinib, the reverse factor was 1. 83 and 2.72-fold respectively. Cell cycle arrested at G2/M phase could be observed by flow cytometry on BOR treatment. The over-expression of COX-2 and mdrl could be down-regulated by BOR. Conclusions BOR can enhance the imatinib sensitivity of imatinib resistant K562/G01 cell. The mechanism may be related to cell cycle phase arrested at G2/M and down-regulation of COX-2 and mdrl expression.