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机构地区:[1]重庆医科大学附属第二医院普外科,重庆400016
出 处:《中国生物制品学杂志》2012年第1期72-77,共6页Chinese Journal of Biologicals
基 金:重庆市科技攻关项目(CSTC;2008AC5082)
摘 要:目的探讨乌司他丁(Ulinastatin,UTI)和泰索帝(Taxotere,TXT)对人原代乳腺癌细胞增殖、侵袭及胰岛素样生长因子受体1(Insulin-like growth factor 1 receptor,IGF-1R)、血小板衍生因子A(Platelet-derived growth factor A,PDGFA)和血小板活化因子受体(Platelet-activating factor receptor,PAFR)表达的影响。方法将原代培养的乳腺癌细胞分为4组:UTI组(800 IU/ml)、TXT组(3.7μg/ml)、UTI+TXT组和培养液对照组,MTT法检测细胞的增殖活力;Transwell小室法检测细胞的侵袭能力;流式细胞仪检测细胞凋亡情况;RT-PCR和Western blot检测细胞中IGF-1R、PDGFA及PAFR基因mRNA的转录水平及蛋白的表达水平。结果 UTI和TXT均可显著抑制人原代乳腺癌细胞的增殖和侵袭能力,诱导细胞凋亡,下调细胞中IGF-1R、PDGFA及PAFR基因mRNA的转录水平和蛋白的表达水平,且UTI与TXT联合使用时效果更为明显。结论 UTI能够增强TXT对人原代乳腺癌细胞的抑制作用,二者具有协同效应,这种机制可能与UTI影响IGF-1R、PDGFA和PAFR的表达有关。Objective To investigate the effect of Ulinastatin (UTI) and Taxotere (TXT) on proliferation and invasion of primary human breast cells as well as expression of insulin-like growth factor 1 receptor (IGF-1R), platelet-derived growth factor A (PDGFA) and platelet-activating factor receptor (PAFR). Methods Primary culture of breast cancer cells were divided into four groups. The cells in three test groups were treated with UTI (800 IU/ml), TXT (3. 7 p^g/ml) and UTI (800 IU/ml ) + TXT (3. 7 I^g/ml) respectively, while those in control group with RPMI1640 medium containing 10% fetal bovine serum, and determined for proliferation activity by MrI'y method, for invasion ability by Transwell test, for apoptosis by flow cytometry, and for expressions of IGF-1R, PDGFA and PAFR at mRNA and protein levels by RT-PCR and Western blot respectively. Results Both UTI and TXT inhibited the proliferation and invasion abilities and induced the apoptosis of primary human breast cancer cells significantly, while down-regulated the expressions of IGF-1R, PDGFA and PAFR at mRNA and protein levels. However, the effect of UTI combined with TXT was superior to that of UTI or TXT alone. Conclusion UTI enhanced the inhibitory effect of TXT on primary human breast cancer cells, and showed synergistic action with TXT, of which the mechanism might be associated with the influence of UTI on expressions of IGF-1R, PDGFA and PAFR.
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