摘要
目的:构建稳定表达NK4的LM3肝癌细胞系,建立裸鼠肝癌模型,观察肿瘤生长情况,并探讨NK4抑制肿瘤可能的机制。方法:构建携带NK4基因的慢病毒载体pLenti6.3-NK4-IRES-EGFP,转染LM3细胞构建稳定表达NK4的细胞系,分组建立裸鼠肝癌皮下移植瘤模型。测量肿瘤瘤体的体积,重量,采用免疫组化等方法观察肿瘤微血管密度,瘤体中MMP-9的表达。结果:接种肝癌细胞28天后,NK4组裸鼠移植瘤体积为(1.28±0.25)cm3,明显小于对照组与空载体组(2.15±0.58)cm3和(2.06±0.51)cm3(P<0.01)。NK4组瘤重为(1.17±0.78)g,显著低于对照组和空载体组(3.69±1.92)g和(3.52±1.68)g(P<0.01)。NK4转染组的肿瘤血管密度为(10.25±3.85),显著低于对照组和空载体组(2 6.5 6±7.6 2)和(24.37±8.34)。NK4组瘤体中MMP-9表达明显减少。结论:转染NK4基因可以显著抑制裸鼠肝癌移植瘤的生长,其作用机制可能是通过抑制肿瘤内新生血管的形成和肿瘤细胞的侵袭。
Objective：The effects and mechanisms of pLenti6.3-NK4-IRES-EGFP on tumor growth and angiogenesis of LM3 xenografts in nude mice were investigated.Methods： PLenti6.3-NK4-IRES-EGFP was constructed and transfected LM3 cells.Nude mice model were established by injecting LM3 cells subcutaneously into the right flank of each mouse.Anti tumor effects of NK4 were investigated by measuring volumes and weights of tumors,observing microvessel density and detecting expression of MMP-9.Results： All mice were euthanized on the 28th day,and the final tumor volume and weight in the NK4 group（1.28±0.25） cm3 and（1.17±0.78）g respectively were markedly smaller than in the null（2.15±0.58） cm3 and（3.69±1.92） g and Lenti-vector group（2.06±0.51） cm3 and（3.52±1.68） g,P〈0.01）.Microvessel density in the NK4 group（10.25±3.85）was markedly lower than in the null group and Lenti-vector group（26.56±7.62 and 24.37±8.34,P〈0.01）.Expression of MMP-9 in NK4 group decreased significantly.Conclusion： LM3 xenografts were significantly inhibited by NK4 by inhibiting tumor angiogenesis and invasion.
出处
《现代肿瘤医学》
CAS
2012年第11期2255-2258,共4页
Journal of Modern Oncology
基金
辽宁省科技厅科学技术计划(No:2009225008-13)
关键词
肝癌
移植瘤
NK4
裸鼠
基因转染
hepatocellular carcinoma
xenograft
NK4
nude mice
gene-transfection
