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目的:体外观察胃癌细胞株形成血管生成拟态(VM)的能力,并通过Mig-7-siRNA转染SGC7901细胞,观察其对VM形成的影响,初步探讨其可能机制。方法:采用体外三维培养技术,在光镜及扫描电镜下观察不同分化程度的胃癌细胞形成VM的能力,并检测迁移诱导蛋白7(Mig-7)表达;通过Mig-7-siRNA转染SGC7901细胞,观察其对VM、侵袭及迁移能力的影响;Western blot检测SGC7901细胞中Mig-7、磷酸化细胞外调节蛋白激酶1、2(p-ERK1/2)及基质金属蛋白酶2(MMP-2)表达。结果:体外实验显示MKN45和SGC7901能形成VM,表达Mig-7;而MKN28和GES-1无形成VM能力,Mig-7表达阴性;Mig-7-siRNA转染SGC7901细胞后可干扰VM形成、侵袭及迁移能力;下调p-ERK1/2和MMP-2蛋白表达,可干扰VM形成。结论:能形成VM的细胞,可表达Mig-7;干扰Mig-7的表达,抑制VM的形成,可能与下调p-ERK1/2和MMP-2蛋白表达有关。
OBJECTIVE: To observe the ability of gastric cancer cell lines to form vasculogenic mimicry (VM) in vitro. SGC7901 cells were transfected with Mig-7-siRNA to observe its effect on VM formation and to explore its possible mechanism. Methods: The ability of VM to differentiate into gastric cancer cells was observed by light microscopy and scanning electron microscopy. The expression of migration-induced protein 7 (Mig-7) was detected. The expression of Mig-7 protein was detected by using Mig-7-siRNA in SGC7901 cells , And their effects on VM, invasion and migration were observed. Western blot was used to detect the expression of Mig-7, p-ERK1 / 2 and MMP-2 in SGC7901 cells, expression. Results: In vitro experiments showed that VMN45 and SGC7901 could form VM and express Mig-7, while MKN28 and GES-1 had no VM ability and negative expression of Mig-7. Mig-7-siRNA transfected SGC7901 cells could interfere with VM formation and invasion And migration ability; downregulation of p-ERK1 / 2 and MMP-2 protein expression, can interfere with VM formation. CONCLUSION: Cells capable of forming VM express Mig-7, interfere with the expression of Mig-7 and inhibit the formation of VM, which may be related to the down-regulation of the expression of p-ERK1 / 2 and MMP-2.