线粒体分裂蛋白MiD51在HBV相关肝癌转移中的调控作用  

Role of mitochondrial fission protein MiD51 in the regulation of metastasis in hepatocellular carcinoma cells

作　　者：刘彦斌[1] 聂娜 李娟[1] 王晓玉[2] 张庆[1] LIU Yan-bin;NIE Na;LI Juan;WANG Xiao-yu;ZHANG Qing(Department of Infectious Diseases, Hanzhong Central Hospital, Hanzhong 723000, Shaanxi, CHINA;Department of Ophthalmology , Hanzhong Central Hospital, Hanzhong 723000, Shaanxi, CHINA)

机构地区：[1]汉中市中心医院感染科,陕西汉中723000 [2]汉中市中心医院眼科,陕西汉中723000

出　　处：《海南医学》2019年第13期1652-1656,共5页Hainan Medical Journal

摘　　要：目的研究线粒体分裂蛋白MiD51在调控HBV相关肝癌转移中的作用。方法(1)分别采用qRT-PCR、Western blot与免疫组化实验,评估15例HBV相关肝癌患者原发灶与转移灶组织中MiD51的表达;(2)利用siRNA下调HBV阳性肝癌细胞中MiD51表达后,用细胞划痕实验分析对肝癌细胞迁移能力的影响;(3)利用siRNA下调HBV阳性肝癌细胞中MiD51表达后,用Transwell侵袭实验分析对肝癌细胞侵袭能力的影响。结果(1)与原发灶相比,转移灶组织中MiD51分子的mRNA与蛋白水平均显著升高[RT-PCR:原发灶 vs 转移灶=(1.00±0.26) vs(2.65±0.31);Western blot:原发灶 vs转移灶=(1.00±0.02) vs (3.32±0.33);免疫组化:(0.43±0.04) vs (0.70±0.06)],差异有统计学意义(P<0.05);(2)下调MiD51表达可显著抑制肝癌细胞的迁移能力[siCtrl vs siMID51#1 vs siMID51#2=(69±2.65)% vs (44±2.40)% vs (43±1.53)%],差异有统计学意义(P<0.05);(3)下调MiD51表达可显著抑制肝癌细胞的侵袭能力[siCtrl vs siMID51#1 vs siMID51#2=(35.33±3.53) vs (16.33±1.86) vs (17.67±2.03)],差异有统计学意义(P<0.05)。结论线粒体分裂蛋白MiD51在HBV阳性肝癌的转移灶组织中表达显著上调,进而促进肝癌细胞的迁移与侵袭能力,提示MiD51是潜在的HBV阳性肝癌诊断与治疗的分子靶标。Objective To explore the role of mitochondrial fission protein MiD51 (mitochondrial dynamic pro-tein of 51 KDa) in the regulation of metastasis in hepatocellular carcinoma (HCC) cells. Methods (1) qRT-PCR, West-ern blot and immunohistochemistry analysis were used to evaluate the expression levels of MiD51 in the primary andmetastatic tumor tissues from 15 HBV positive HCC patients.(2) The effect of MiD51 knockdown by small interferingRNA (siRNA) on the migration ability of HBV positive HCC cells was evaluated by the scratch wound healing assay.(3)The effect of MiD51 knockdown by small interfering RNA (siRNA) on the invasion ability of HBV positive HCC cellswas evaluated by the transwell invasion assay. Results (1) Compared with primary tumor tissues, the expression ofMiD51 was significantly higher in the metastatic tumor tissues of HBV positive HCC: qRT-PCR: primary tissue vs meta-static tissue=(1.00±0.26) vs (2.65±0.31);Western blot: Primary tissue vs Metastatic tissue=(1.00±0.02) vs (3.32±0.33);Im-munohistochemistry: primary tissue vs Metastatic tissue=(0.43 ± 0.04) vs (0.70 ± 0.06);all P<0.05.(2) Knockdown ofMiD51 dramatically inhibited the migration ability of HBV positive HCC cells: siCtrl vs siMID51#1 vs siMID51#2=(69±2.65)% vs (44±2.40)% vs (43±1.53)%, all P<0.05.(3) Knockdown of MiD51 clearly inhibited the invasion ability ofHBV positive HCC cells: siCtrl vs siMID51#1 vs siMID51#2=(35.33±3.53) vs (16.33±1.86) vs (17.67±2.03), all P<0.05.Conclusion Compared with primary tumor tissues, the expression of MiD51 is significantly elevated in the metastatictumor tissues of HBV positive HCC, which promotes both migration and invasion of HCC cells, suggesting MiD51 as apotential therapeutic target in the treatment of HBV positive HCC.

关 键 词：线粒体分裂 线粒体分裂蛋白51 肝癌 迁移 侵袭 

分 类 号：R735.7[医药卫生—肿瘤]