摘要
目的探讨中期因子(MDK)在肝细胞肝癌(HCC)中的表达及对肿瘤细胞增殖、凋亡及侵袭能力的影响。方法选取2015年1月-2016年10月该院收治的50例肝癌患者组织标本,免疫组织化学染色分析组织中MDK的表达。利用沉默核糖核酸(si RNA)沉默人肝细胞癌HepG2细胞内MDK表达,分别采用CCK-8、流式细胞仪及插入式细胞培养皿、穿透小室(Transwell)检测沉默MDK后HepG2细胞增殖、凋亡及侵袭能力变化。结果肝癌组织中MDK蛋白的表达水平较癌旁组织提高(χ~2=19.643,P=0.000);在HepG2细胞中,沉默MDK的表达可抑制HepG2细胞增殖(F=22.204,P=0.037)和侵袭(t=5.611,P=0.008)能力,并提高HepG2细胞的凋亡比例(t=5.702,P=0.006)。结论 MDK在肝癌中表达升高,沉默肝癌HepG2细胞内MDK表达能够抑制肝癌细胞生长和侵袭。
Objective To study the expression and roles of midkine （MDK） in human hepatocellular carcinoma （HCC）. Methods A total of 50 HCC tissues and tumor adjacent tissues were collected to detect the expression of MDK by immunohistochemieal staining. The expression of MDK in HepG2 cells was silenced by siRNA. Cell proliferation, apoptosis and invasion were detected by CCK-8, flow cytometry and Transwell, respectively. Results MDK expression was up-regulated in HCC tissues （P〈 0.05）. Knockdown MDK in HCC cells was significantly down-regulated cell proliferation, invasion and induced apoptosis. Conclusions MDK is over-expressed in HCC tissues. Knockdown MDK can inhibit growth and invasion on HepG2 cells.
出处
《中国现代医学杂志》
CAS
北大核心
2017年第11期36-40,共5页
China Journal of Modern Medicine
关键词
中期因子
肝细胞癌
增殖
凋亡
侵袭
MDK
hepatocellular carcinoma
proliferation
apoptosis
invasion
