miR-21通过PDCD4调控肝癌细胞的生长和侵袭

摘要

Purpose To evaluate the expression of miR-21 in the tissues and cell lines of hepatocellular carcinoma,and to try to find its possible target genes.Methods The expression profile of miR-21 was detected in hepatocellular carcinoma tissues and cell lines.Mter miR-21 inhibitor was used,the alterations in the vitality and invasion of hepatocellular carcinoma cells were observed.The possible target gene of miR-21 was predicted by bioinformatics analysis.The influence of miR-21 inhibitors on the target gene activity was evaluated by dual luciferase reporting gene system.Results The expression level of miR-21 was significantly higher in hepatocellular carcinoma tissues than that in the adjacent ones (P ＜0.05).The expression level of miR-21 in hepatocellular carcinoma cells was significantly higher than that in the hepatic cells (P ＜0.01).After inhibiting miR-21,the viability and invasion ability of hepatocellular carcinoma cells were decreased (P ＜ 0.01).The expression level of programmed cell death 4 (PDCD4) in hepatocellular carcinoma tissues was significantly lower than that in the adjacent tissues (P ＜ 0.01).Its expression level in hepatocellular carcinoma cells was significantly lower than that in the hepatic cells (P ＜ 0.01).After interfering with PDCD4,the vitality and invasion ability of liver cancer cells were increased (P ＜ 0.05).Dual luciferase reporter gene assay indicated that by inhibiting miR-21,the expression level of PDCD4 was up-regulated (P ＜ 0.01).The vitality and invasion ability of liver cancer cells were reduced (P ＜ 0.001).Conclusion MiR-21 can regulate the growth and invasion of liver cancer cells through targeting PDCD4.%目的 探讨miR-21在原发性肝细胞癌(hepatocellular carcinoma,HCC)组织和细胞中的表达及其可能调控的靶基因.方法 检测miR-21在HCC组织和细胞系中的表达,使用miR-21抑制剂后,观察HCC细胞活力和侵袭能力的变化;运用生物信息学分析预测miR-21可能的靶基因.应用miR-21抑制剂后,双荧光素酶报告基因系统检测其对靶基因活性的影响.结果 HCC组织中miR-21表达水平显著高于癌旁组织(P ＜0.05);HCC细胞中miR-21的表达水平显著高于肝细胞(P＜0.01).抑制miR-21后,HCC细胞的活力和侵袭能力降低(P＜0.01).抑癌基因程序性死亡因子4(programmed cell death 4,PDCD4)在HCC组织中的表达显著低于癌旁组织(P＜0.01),在肝癌细胞中的表达水平显著低于肝细胞(P＜0.01).干扰PDCD4后,肝癌细胞的活力和侵袭能力提高(P＜0.05).双荧光素酶报告基因检测显示,使用miR-21抑制剂后,PDCD4表达上调(P＜0.01),肝癌细胞的侵袭和增殖能力降低(P＜0.01).干扰PDCD4后,肝癌细胞的侵袭和增殖能力升高(P＜0.001).结论 miR-21可通过PDCD4调控肝癌细胞的生长和侵袭.