转录因子Sp1调控VEGF和MMP2的表达促进NK/T细胞淋巴瘤的侵袭

Sp1 promotes cell invasion by up-regulation of VEGF and MMP2 expression in NK/T-cell lymphoma cells

目的:检测转录因子Sp1在NK/T细胞淋巴瘤(NK/TCL)细胞株中的表达,探讨Sp1对肿瘤细胞侵袭的作用及其可能的调控机制。方法:利用Real-time PCR、免疫荧光技术和蛋白质免疫印迹技术检测Spl的表达,Real-time PCR技术和蛋白质免疫印迹技术检测血管内皮生长因子(VEGF)和基质金属蛋白酶(MMP)2的表达,Transwell技术观察Sp1抑制剂光神霉素A(MIT)对细胞侵袭能力的影响。结果:NK/TCL细胞株SNK-1、SNK-6和SNT-8均高表达Sp1。MIT显著抑制SNK-1、SNK-6和SNT-8中VEGF基因和蛋白水平的表达,MMP2蛋白的表达以及细胞的侵袭能力。结论:NK/TCL肿瘤细胞株中存在高表达的Sp1,并可促进肿瘤细胞的侵袭。Sp1可通过调控VEGF和MMP2的表达影响细胞的侵袭力。

Objective：To identify the expression of Spl in NK/T-cell lymphoma （NK/TCL） cell lines and to investigate the role of Sp1 in regulation of cell invasion. Method：Real-time PCR,immunofluorescence and Western blot were performed to detect the expression of Sp1. Expression levels of VEGF and MMP2 were measured by Real-time PCR and Western blot,respectively. Transwell assay was applied to observe the effects of mythramycin A （MIT） on cell invasion. Result： Sp1 was identified over-expression in three NK/TCL cell lines as compared with that of NK cells from healthy donors. Inhibition of Sp1 by MIT remarkably reduced expression of VEGF and MMP2 in SNK-1, SNK-6 and SNT-8, and as a result it significantly suppressed cell invasion. Conclusion： Sp1 is over-expressed in NK/TCL cells, and promotes NK/TCL cell invasion by up-regulating the expression of VEGF and MMP2.