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首页|期刊导航|临床神经外科杂志|AKT2在胶质瘤细胞中替莫唑胺化疗耐药的作用机制研究

AKT2在胶质瘤细胞中替莫唑胺化疗耐药的作用机制研究

崔勇 张风林 应奇 胡国汉 骆纯 卢亦成

临床神经外科杂志2017,Vol.14Issue(1):26-29,4.
临床神经外科杂志2017,Vol.14Issue(1):26-29,4.DOI:10.3969/j.issn.1672-7770.2017.01.007

AKT2在胶质瘤细胞中替莫唑胺化疗耐药的作用机制研究

The role of AKT2 in resistance totemozolomide in glioma cell line U251

崔勇 1张风林 1应奇 1胡国汉 2骆纯 2卢亦成2

作者信息

  • 1. 200081 上海,解放军第411医院神经外科
  • 2. 第二军医大学附属长征医院神经外科
  • 折叠

摘要

Abstract

Objective To explore the effects of AKT2 expression in U251 glioma cells on the sensitivity towards to temozolomide ( TMZ).Methods The lentivirus vector of AKT2 shRNA was constructed and transfected into U251 cells.The changes of TMZ sensitivity after shRNA were examined by the CCK8 assay.Apoptosis of cells of each group was detected by flow cytometry cell technology.further analysis and evaluation of the AKT2 and the MDR-1, MRP-1, MGMT, and apoptosis related protein expression regulatory interaction used by Real-time PCR and Western Blot . Results the IC50 of U251 cell decreased from the blank control group (39.72 ±2.41)μg/ml, negative control group (39.43 ±2.24)μg/ml to (27.23 ±1.93) μg/ml,sensitivity of U251 cell to TMZ decreased significantly .Western blot results showed Bcl-2, survivin, MGMT was down regulated,and Caspase-3,PTEN,P53,beclin-1 increased.Conclusion AKT2 may be involved in the regulation of expression of apoptosis and autophagy related protein Bcl-2, Caspase-3, P53, survivin, Beclin1, and DNA damage repair protein MGMT , which mediates U251 chemotherapy resistance to TMZ.

关键词

脑胶质瘤/AKT2基因/替莫唑胺

Key words

glioma/AKT2/temozolomide

分类

医药卫生

引用本文复制引用

崔勇,张风林,应奇,胡国汉,骆纯,卢亦成..AKT2在胶质瘤细胞中替莫唑胺化疗耐药的作用机制研究[J].临床神经外科杂志,2017,14(1):26-29,4.

基金项目

国家自然科学基金 ()

临床神经外科杂志

OACSTPCD

1672-7770

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