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目的观察乌斯他丁(UTI)和环磷酰胺(CTX)对体外培养的乳腺癌细胞MCF-7(雌激素受体阳性)和乳腺癌细胞MDA-MB-231(雌激素受体阴性)增殖、侵袭及基质金属蛋白酶-9(MMP-9)表达的影响。方法将体外培养的乳腺癌细胞MCF-7和MDA-MB-231分别分为8组:对照组、UTI高、中、低剂量组、CTX组、CTX+UTI高、中、低剂量组,分别用相应药物处理。采用MTT法检测细胞的增殖能力;流式细胞仪分析细胞周期;RT-PCR检测细胞MMP-9基因的表达;Boyden小室侵袭试验检测两种细胞的浸袭能力。结果UTI可明显抑制MCF-7和MDA-MB-231细胞的增殖,使细胞周期阻滞在G2/M期,并能使2株细胞中MMP-9基因的转录水平下降,细胞的增殖侵袭能力降低。CTX与UTI联合应用,其作用效果优于CTX单独使用。结论UTI能增强CTX诱导的乳腺癌细胞MCF-7和MDA-MB-231的增殖抑制作用,二者具有协同效应。其机制可能与UTI降低细胞MMP-9基因的表达等有关。
Objective To investigate the effects of UTI and CTX on the proliferation of breast cancer cell line MCF-7 (estrogen receptor positive) and breast cancer cell line MDA-MB-231 (estrogen receptor negative) in vitro , Invasion and the expression of matrix metalloproteinase-9 (MMP-9). Methods The MCF-7 and MDA-MB-231 cells were divided into 8 groups: control group, UTI high, medium and low dose groups, CTX group and CTX + UTI high, medium and low dose groups With the appropriate drug treatment. Cell proliferation was measured by MTT assay. Cell cycle was analyzed by flow cytometry. MMP-9 gene expression was detected by RT-PCR. Boyden chamber invasion assay was used to detect the ability of the two cells to soak. Results UTI significantly inhibited the proliferation of MCF-7 and MDA-MB-231 cells, arresting the cell cycle in G2 / M phase and decreasing the transcription level of MMP-9 gene and the ability of cell proliferation and invasion reduce. CTX and UTI combined application, its effect is better than CTX alone. Conclusion UTI can enhance the CTX-induced proliferation inhibition of breast cancer cells MCF-7 and MDA-MB-231, both of which have a synergistic effect. Its mechanism may be related to UTI to reduce the expression of MMP-9 gene.