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siRNA下调Gli基因影响食管腺癌OE33细胞生长转移的实验研究

王雷 杜媛鲲 刘庆熠 米源 廖海江 王林

中国现代医学杂志2018,Vol.28Issue(8):18-22,5.
中国现代医学杂志2018,Vol.28Issue(8):18-22,5.DOI:10.3969/j.issn.1005-8982.2018.08.004

siRNA下调Gli基因影响食管腺癌OE33细胞生长转移的实验研究

Silencing Gli gene with siRNA modulates growth and invasion of esophageal adenocarcinoma OE33 cells

王雷 1杜媛鲲 2刘庆熠 1米源 1廖海江 1王林1

作者信息

  • 1. 河北医科大学第四医院 胸二科,河北 石家庄 050011
  • 2. 河北医科大学 期刊社,河北 石家庄 050017
  • 折叠

摘要

Abstract

Objective To explore the effect of down-regulation of Gli expression on growth and invasion of esophageal adenocarcinoma OE33 cells and to discuss the molecular mechanisms. Methods Gli1 and Gli2 siRNA and control siRNA were respectively transfected into OE33 cells for 48 h.Expressions of the Gli1 and Gli2 mRNA and protein were detected by real-time fluorescence quantitative PCR and Western blot respectively. The expressions of cyclin D1, p27, E-cadherin and N-cadherin proteins were observed by Western blot. The cell cycle was determined by flow cytometry.In addition,invasion ability was detected by Transwell assay. Results After transfection of Gli1 and Gli2 siRNA,Gli1 and Gli2 expressions were inhibited,the expressions of cyclin D1 and N-cadherin proteins were downregulated, and E-cadherin and p27 expressions were increased (P< 0.05).After Gli1 and Gli2 were knocked down, cell cycle was arrested at G0/G1 phase and cell invasion ability was decreased compared with the control siRNA(P<0.05). Conclusions Gli may play an important role in the growth and invasion of esophageal adenocarcinoma.Gli1 and Gli2 knockout can inhibit the cell cycle and epithelial-mesenchymal transition,which may be associated with cyclin D1, p27, E-cadherin and N-cadherin.

关键词

RNA干扰/食管腺癌/Gli/细胞周期/上皮-间质转化

Key words

RNA interference/esophageal adenocarcinoma/Gli/cell cycle/epithelial-mesenchymal transition

分类

医药卫生

引用本文复制引用

王雷,杜媛鲲,刘庆熠,米源,廖海江,王林..siRNA下调Gli基因影响食管腺癌OE33细胞生长转移的实验研究[J].中国现代医学杂志,2018,28(8):18-22,5.

基金项目

河北省科技计划项目(No:132077127D) (No:132077127D)

河北省卫生厅医学科学研究重点课题(No:20160177) (No:20160177)

中国现代医学杂志

OACSTPCD

1005-8982

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