迁移诱导蛋白7促进胃癌血管生成拟态

Mig-7 enhances vasculogenic mimicry in gastric cancer cells

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。

AIM： To observe vasculogenic mimicry （VM） in gastric cancer cells in vitro, and explore the possible underlying mechanisms by transfecting SGC7901 cells with Mig-7-siRNA and observing the impact on VM formation. METHODS： The capability of VM formation in differently differentiated gastric cancer cells were observed by light microscopy and scanning electron microscopy in a three- dimensional culture system. The expression of Mig-7 was detected. The impact of transfection with Mig-7-siRNA into SGC7901 cells on the abilities of VM formation, invasion and migration were also examined. The expressions of Mig-7, phosphor-extracellular regulated protein kinases 1, 2 （p- ERKI/2） and matrix metalloproteinase-2 （MMP-2） in SGC7901 cells were analyzed by Western blotting. RESULTS： VM formation was observed in poorly differentiated MKN45 and moderately differentiated SGC7901 cells, but not in well differentiated MKN28 and normal GES-1 cells in vitro; Mig-7 was expressed in MKN45 and SGC7901 cells, but not in MKN28 and GES-1 cells; the abilities of VM formation, invasion and migration were changed by trans- fection with Mig-7-siRNA into SGC7901 cells. The formation of VM was reduced by down-regulating the expressions of p-ERK1/2 and MMP-2 protein in SGC7901 cells. CONCLU- SION： Mig-7 is expressed in gastric cancer cells which are able to form VM. The formation of VM is inhibited by reducing the expression of Mig-7 in gastric cancer cells, which might be mediated by down-regulating the expres- sions of p-ERK1/2 and MMP-2 proteins.