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TAT-N24穿膜融合多肽对HepG2细胞增殖的影响

Inhibition of cell-permeable TAT-N24 fusion peptide on proliferation of HepG2 cells in vitro
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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。 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%(P0.05),respectively;the percentages of G0/G1 phase cells were 52.6±4.7%,52.0±4.6% and 68.6±4.7%(P0.05),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.
出处 《实用肝脏病杂志》 CAS 2011年第5期321-322,326,共3页 Journal of Practical Hepatology
基金 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)
关键词 HEPG2细胞 TAT-N24穿膜融合多肽 分子靶向治疗 HepG2 cells Cell-permeable TAT-N24 fusion peptide Molecular targeting therapy
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  • 1高霞,龙浩成,刘双又,罗学来,李小兰,陶德定,胡俊波,龚建平.信号传导途径p55PI3K-Rb在胃肠道肿瘤中的表达及意义[J].华中科技大学学报(医学版),2006,35(6):761-763. 被引量:9
  • 2陶站华,王淑静,刘兴汉.蛋白质转导技术及其应用[J].医学分子生物学杂志,2005,2(2):119-122. 被引量:2
  • 3刘双又,王晶,高霞,罗学来,谢大兴,冯永东,陶德定,胡俊波,龚建平.磷脂酰肌醇-3激酶上的一段多肽对Jurkat细胞的周期阻滞作用[J].中华血液学杂志,2005,26(12):758-759. 被引量:6
  • 4王晶,刘双又,高霞,罗学来,夏献民,陶德定,龚建平,胡俊波.N24p55γPI3K靶向抑制胃癌细胞增殖的研究[J].中华实验外科杂志,2006,23(10):1221-1223. 被引量:13
  • 5KAELIN W J.Functions of the retinoblastoma protein[J].Bioessays,1999,21(11):950-958.
  • 6VANHAESEBROECK B,LEEVERS S J,PANAYOTOM G,et al.Phosphoinositide 3-kinases:a conserved family of signal transducers[J].Trends Biochem Sci,1997,22 (7):267-272.
  • 7XIA X,CHENG A,AKINMADE D,et al.The N-terminal 24 amino acids of the p55 gamma regulluatory subunit of phosphoinositide 3-kinase hinds Rb and induces cell cycle arrest[J].Mol Cell Biol,2003,23(5):1717-1725.
  • 8HU J B,LIU S,WANG J,et al.Overexpression of the Nterminal end of the 055γ regulatory subunit of phosphatidylinositol 3-kinase blocks cell cycle progression in gastric carcinoma cells[J].Int J Oncol,2005,26(5):1321-1327.
  • 9LUO J,MANNING B D,CANTLEY L C.Targeting the PI3K-Akt pathway in human cancer:rationale and promise[J].Cancer Cell,2003,4(4):257-262.
  • 10WARD S G,FINAN P.Isoform-specific phosphoinositide 3-kinase inhibitors as therapeutic agents[J].Curr Opin Pharmacol,2003,3 (4):426-434.

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