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DCN调控TGF-βRII高表达抑制HepG2细胞增殖分子机制研究

刘岩峰 王大伟 鞠文博 任爱华

北华大学学报(自然科学版)2017,Vol.18Issue(6):735-739,5.
北华大学学报(自然科学版)2017,Vol.18Issue(6):735-739,5.DOI:10.11713/j.issn.1009-4822.2017.06.007

DCN调控TGF-βRII高表达抑制HepG2细胞增殖分子机制研究

On the Proliferation of HepG2 Cells Inhibited by Strongly Expressed TGF-βRII Regulated by DCN

刘岩峰 1王大伟 1鞠文博 1任爱华1

作者信息

  • 1. 北华大学医学部,吉林吉林 132013
  • 折叠

摘要

Abstract

Objective To discuss the molecular mechanism of the proliferation of human HepG2 cells inhibited by DCN through transforming growth factor-β(TGF-β)signaling pathway. Method A vector containing DCN was transfected into HepG2 cells with the use of Lipofectamine 2000 . Cell proliferation was assessed with an MTT assay,and western blot analysis was used to detect the protein expression of TGF-β receptor I (TGFβRI ), phosphorylated TGFβRI,p15 and TGFβRII. In addition,small interfering RNA (siRNA)silencing was performed to knock down the target gene. Results Cell proliferation was significantly decreased in HepG2 cells transfected with DCN. In addition,DCN transfection significantly increased the phosphorylation level of TGFβRI in HepG2 cells. Compared with the control group,the expression of the downstream factor p15 was also significantly elevated in the DCN transfected HepG2 cells (P<0 . 05 ). Conclusion DCN transfection significantly elevated the expression level of TGFβRII in HepG2 cells. And the usage of siRNA can weaken this phenomenon.

关键词

DCN/细胞增殖/抗肿瘤/HepG2/TGF-β

Key words

DCN/cell proliferation/antineoplastic/HepG2/TGF-β

分类

医药卫生

引用本文复制引用

刘岩峰,王大伟,鞠文博,任爱华..DCN调控TGF-βRII高表达抑制HepG2细胞增殖分子机制研究[J].北华大学学报(自然科学版),2017,18(6):735-739,5.

基金项目

吉林省卫生技术创新项目(2016J084) (2016J084)

吉林省教育厅科学技术研究项目. ()

北华大学学报(自然科学版)

OACSTPCD

1009-4822

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