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为了探讨酪氨酸激酶抑制剂STI571对RPMI8226细胞黏附、黏附诱导耐药以及靶细胞Rac1mRNA表达的影响,本研究采用结晶紫染色法分析了RPMI8226细胞与纤连蛋白(fibronectin,FN)的黏附率,用MTT法检测瘤细胞的增殖性,并用半定量RT-PCR研究Rac1mRNA水平的变化。结果显示:RPMI8226细胞与FN黏附1、6、12小时,其黏附率分别为(43.71±2.18)%、(55.63±1.56)%、(63.42±2.46)%;用20μmol/LSTI571处理1、6、12小时后黏附率分别降为(15.12±1.04)%、(17.58±1.32)%、(17.24±1.59)%;组间差异显著(P<0.05);阿霉素作用后,FN黏附组细胞IC50值[(1.46±0.04)μmol/L]显著高于BSA组[(0.78±0.03)μmol/L](P<0.05);FN联合STI571组IC50值[(0.81±0.05)μmol/L]与BSA联合STI571组[(0.74±0.02)μmol/L]相比无显著性差异(P>0.05),但却低于FN组(P<0.05);半定量RT-PCR显示,Rac1mRNA水平在20μmol/LSTI571处理14小时后明显下降。结论:STI571能降低RPMI8226细胞与FN的黏附率、逆转黏附介导的阿霉素耐药,并且可以下调其Rac1mRNA水平。
In order to investigate the effect of STI571, a tyrosine kinase inhibitor, on the adhesion and adhesion-promoting drug resistance of RPMI8226 cells and the expression of Rac1 mRNA in RPMI8226 cells, the adhesion rate of RPMI8226 cells to fibronectin (FN) The proliferation of tumor cells was detected by MTT assay, and the changes of Rac1 mRNA level by semi-quantitative RT-PCR. The results showed that the adhesion rates of RPMI8226 cells to FN for 1, 6, 12 hours were (43.71 ± 2.18)%, (55.63 ± 1.56)%, (63.42 ± 2.46)%, respectively. After 12 hours, the adherent rate decreased to (15.12 ± 1.04)%, (17.58 ± 1.32)% and (17.24 ± 1.59)%, respectively. The difference between the two groups was significant (1.46 ± 0.04) μmol / L] was significantly higher than that of BSA group [(0.78 ± 0.03) μmol / L] (P <0.05) (P <0.05), but lower than that of FN group (P <0.05). Semi-quantitative RT-PCR showed that the level of Rac1 mRNA in 20μmol / LSTI571 group was significantly higher than that in STI571 group [(0.74 ± 0.02) μmol / L] Significant decrease after 14 hours of treatment. CONCLUSIONS: STI571 can reduce the adherence rate of RPMI8226 cells to FN, reverse the adhesion-mediated doxorubicin resistance and down-regulate the Rac1 mRNA level.