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ITIH4基因沉默对人肝癌细胞HepG2增殖、迁移及侵袭的影响

段煜 姜文文 高鹏 唐泽耀

临床与病理杂志2017,Vol.37Issue(7):1325-1330,6.
临床与病理杂志2017,Vol.37Issue(7):1325-1330,6.DOI:10.3978/j.issn.2095-6959.2017.07.001

ITIH4基因沉默对人肝癌细胞HepG2增殖、迁移及侵袭的影响

Effect of ITIH4 gene silence on proliferation, migration and invasion of human hepatocellular carcinoma cell HepG2

段煜 1姜文文 1高鹏 2唐泽耀3

作者信息

  • 1. 大连医科大学附属第六人民医院肝病科,辽宁 大连 116044
  • 2. 大连医科大学附属第六人民医院检验科,辽宁 大连 116044
  • 3. 大连医科大学药理学教研室,辽宁 大连 116044
  • 折叠

摘要

Abstract

Objective: To investigate the effect of inter-alpha-trypsin inhibitor heavy chain H4 gene silence on proliferation, migration and invasion of human hepatocellular carcinoma cell HepG2.Methods: Four ITIH4 silencing vectors were delivered in to HepG2 cells by transfection. Stable cell clones were selected by 2 μg/mL puromycin. Silencing efficiency was evaluated by Western Blot and cell clone with the highest silencing efficacy (si-ITIH4) was used in the following study. Cell clone transfected with scramble sequence was used as normal control (si-Control). Cell counting and CCK-8 assay were applied to assess cell proliferation. Transwell assay was performed to evaluate cell migration and invasion.Results: We successfully obtained a HepG2 cell line with ITIH4 gene silencing named si-ITIH4. The silencing efficiency was 86% in compassion with si-Control. Compared to the si-Control group, si-ITIH4 cells showed significantly slower proliferation, decreased migration and mitigated invasion.Conclusion: Silence of ITIH4 significantly inhibited proliferation, migration and invasion of HepG2 cells. This study suggests that ITIH4 might be essentially involved in onset and progression of hepatocellular carcinoma.

关键词

间-α-胰蛋白酶抑制剂重链H4/增殖/迁移/侵袭/肝细胞癌

Key words

inter-alpha-trypsin inhibitor heavy chain H4/proliferation/migration/invasion/hepatocellular carcinoma

引用本文复制引用

段煜,姜文文,高鹏,唐泽耀..ITIH4基因沉默对人肝癌细胞HepG2增殖、迁移及侵袭的影响[J].临床与病理杂志,2017,37(7):1325-1330,6.

基金项目

辽宁省自然科学基金(201602206).This work was supported by Nature Science Foundation of Liaoning Province, China (201602206). (201602206)

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