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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 effects of Ulinastatin (UTI) and Taxotere (TXT) on the proliferation and invasion of human primary breast cancer cells and the effects of insulin-like growth factor 1 receptor (IGF-1R ), Platelet-derived growth factor A (PDGFA) and platelet-activating factor receptor (PAFR) were detected by flow cytometry. Methods Primary cultured breast cancer cells were divided into 4 groups: UTI group (800 IU / ml), TXT group (3.7μg / ml), UTI + TXT group and culture medium control group. Transwell chamber assay was used to detect cell invasion. Cell apoptosis was detected by flow cytometry. The mRNA and protein levels of IGF-1R, PDGFA and PAFR were detected by RT-PCR and Western blot. Results Both UTI and TXT significantly inhibited the proliferation and invasion of human primary breast cancer cells, induced apoptosis, down-regulated the mRNA transcription and protein expression of IGF-1R, PDGFA and PAFR, Combined effect is more obvious. Conclusions UTI can enhance the inhibitory effect of TXT on human primary breast cancer cells. Both of them have a synergistic effect, which may be related to the effect of UTI on the expression of IGF-1R, PDGFA and PAFR.