实用肝脏病杂志 ›› 2011, Vol. 14 ›› Issue (5): 321-322.doi: 10.3969/j.issn.1672-5069.2011.05.001

• 论著 •    下一篇

TAT-N24穿膜融合多肽对HepG2细胞增殖的影响*

邓豫,王桂华,金源,李小兰,陶德定,李维娜,龚建平,胡俊波   

  1. 430030 武汉市 华中科技大学同济医学院附属同济医院肿瘤研究所/胃肠外科(邓豫,王桂华,金源,李小兰,陶德定,龚建平,胡俊波);感染性疾病研究所(李维娜)
  • 收稿日期:2011-03-21 出版日期:2011-10-15 发布日期:2016-04-14
  • 通讯作者: 胡俊波,E-mail: jbhu@tjh.tjmu.edu.cn
  • 作者简介:邓豫 男,29岁,博士研究生。主要从事外科学和分子生物学研究。E-mail:leojokea@yahoo.com.cn
  • 基金资助:
    国家973计划项目 (No.2009CB521802);国家自然科学基金资助项目(No. 30872472,30973496,30800569);湖北省自然科学基金资助项目(No. 2008CDB174,2009CDB239)

Inhibition of cell-permeable TAT-N24 fusion peptide on proliferation of HepG2 cells in vitro

DENG Yu,WANG Guihua,JIN Yuan,et al.   

  1. Cancer Research Institute/Department of General Surgery,Tongji Hospital of Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China
  • Received:2011-03-21 Online:2011-10-15 Published:2016-04-14

摘要: 目的 观察TAT-N24穿膜融合多肽对肝癌细胞增殖的抑制作用。方法 用纯化的TAT-N24穿膜融合多肽处理HepG2细胞,使用流式细胞仪检测细胞周期;采用BrdU掺入法检测细胞DNA合成;采用Western Blot法检测细胞内相关蛋白的表达水平。结果 空白组、对照多肽组和TAT-N24处理组细胞BrdU掺入阳性率分别为42.7±3.6%、38.2±2.8%和25.3±2.7%(P<0.05);G0/G1期细胞比例分别为52.6±4.7%、52.0±4.6%和68.6±4.7%(P<0.05);三组细胞AKT磷酸化水平无显著性差异。结论 TAT-N24穿膜融合多肽能有效阻滞肝癌HepG2细胞的细胞周期进程,抑制DNA合成。TAT-N24穿膜融合多肽有望被开发为有效的肿瘤分子靶向治疗药物。

关键词: HepG2细胞, TAT-N24穿膜融合多肽, 分子靶向治疗

Abstract: Objective To investigate the anti-proliferation effects of cell-permeable TAT-N24 fusion peptide in hepatoma cell line. Methods HepG2 cells were treated with cell-permeable TAT-N24 fusion peptide. The cell cycle was analyzed by flow cytometry,the proliferation of the cells was assayed by BrdU incorporation and the expression of phosphorylated AKT was detected by Western blot. Results The incorporation rates of BrdU in blank,control and TAT-N24 group were 42.7±3.6%,38.2±2.8% and 25.3±2.7%(P<0.05),respectively;the percentages of G0/G1 phase cells were 52.6±4.7%,52.0±4.6% and 68.6±4.7%(P<0.05),respectively;the phosphorylation of AKT in the three groups was not significantly different. Conclusion Cell-permeable TAT-N24 fusion peptide effectively inhibites the DNA synthesis and induces cell cycle blocked at G0/G1 phase of HepG2 cells.

Key words: HepG2 cells, Cell-permeable TAT-N24 fusion peptide, Molecular targeting therapy