| 注册
首页|期刊导航|山东医药|UHRF1表达下调对胃癌细胞增殖的抑制作用及机制

UHRF1表达下调对胃癌细胞增殖的抑制作用及机制

类维振 耿亚楠 韩东升 张伟 周林

山东医药2016,Vol.56Issue(21):7-9,3.
山东医药2016,Vol.56Issue(21):7-9,3.DOI:10.3969/j.issn.1002-266X.2016.21.003

UHRF1表达下调对胃癌细胞增殖的抑制作用及机制

Inhibitory effect of down-regulated expression of UHRF1 on cell proliferation of gastric cancer

类维振 1耿亚楠 1韩东升 1张伟 1周林1

作者信息

  • 1. 中国人民解放军第八十八医院,山东泰安 271000
  • 折叠

摘要

Abstract

Objective To investigate the inhibitory effect of down-regulated expression of ubiquitin-like with PHD and ring finger domain 1 (UHRF1)on cell proliferation of gastric cancer (GC)and to explore its mechanism.Methods The gastric cancer cell line (MKN45)were randomly divided into the blank control group,the negative control group (shNC group)and the interference group (shUHRF1 group);the latter two group were infected with shNC and shUHRF1.After UHRF1 expression was down-regulated by shRNA in MKN45 cells,the cell growth was examined by XTT and the clone for-mation rate was calculated by plate clone formation assay.Cell cycle and apoptosis of MKN45 cells were detected by flow cytometry (FCM).In vivo tumorigenicity assay was conducted to examine growth ability in vivo.Results After UHRF1 expression was down-regulated in MKN45 cells by shRNA,the cell growth significantly decreased and colony formation re-duced (all P <0.05).In the shUHRF1 group,the proportion of cells in G0 /G1 phase increased and in S phase de-creased,the apoptosis rate was increased and the difference was statistically significant (all P <0.05).The tumor growth rate in nude mice was significantly decreased (P <0.01).Conclusion The down-regulation of UHRF1 expression may inhibit the proliferation of gastric cancer possibly through extending the cell cycle progression and inducing cell apoptosis.

关键词

胃肿瘤/泛素样含PHD和环指域1/细胞增殖/细胞凋亡

Key words

gastric neoplasms/ubiquitin-like with PHD and ring finger domain 1/cell proliferation/apoptosis

分类

医药卫生

引用本文复制引用

类维振,耿亚楠,韩东升,张伟,周林..UHRF1表达下调对胃癌细胞增殖的抑制作用及机制[J].山东医药,2016,56(21):7-9,3.

基金项目

国家自然科学基金资助项目(81402337)。 ()

山东医药

OA北大核心CSTPCD

1002-266X

访问量0
|
下载量0
段落导航相关论文