期刊文献+

高表达ΔNp73基因对大肠癌细胞生物学行为的影响及其机制研究

Impact of ΔNp73 Expression on Biological Activity of Human Colon Cancer
下载PDF
导出
摘要 目的通过增强肿瘤细胞中外源性ΔNp73基因的表达,探讨该基因对大肠癌细胞生物学行为的影响。方法以人类大肠癌细胞株LOVO细胞为研究对象,将ΔNp73基因用脂质体法转染LOVO细胞,进行细胞生长曲线和流式细胞术分析,测定转染ΔNp73基因后的LOVO细胞的增殖能力与凋亡率;以Boyden小室体外侵袭实验检测ΔNp73基因转染前后LOVO细胞侵袭力变化,并用Western-blot法检测VEGF蛋白的表达。结果转染了ΔNp73基因后的LOVO细胞生长速度较未转染ΔNp73的LOVO细胞明显加快(P<0.01),凋亡率降低;Boyden小室体外侵袭实验显示LOVO-ΔNp73细胞穿膜数较空白对照组和LOVO-pcDNA3组增多,差异具有统计学意义(P<0.01)。与空白对照组相比,LOVO-ΔNp73细胞中VEGF表达较未转染ΔNp73基因的细胞明显增高(P<0.01)。结论ΔNp73过表达促进了大肠癌细胞的增殖和血管生成,增强了大肠癌的侵袭力。 Objective To investigate the relationship between the expression of △Np73 and the invasiveness of human colon cancer. Methods This study we used LOVO cell,a kind cell of human colon cacinoma cell, as the study objective. △Np73 was transferred into LOVO cell by liposome. The effect of △Np73 gene on cell growth was detected by trypan blue counter measurement, cell growth curve and flow cytometry, and invasive ability was assessed with Boyden chamber. Western-blot were employed to detect the expression of VEGF. Results The growth of LOVO-△Np73 cells were significantly increased, the invasive cell number was significantly larger in LOVO-△Np73 cells than in untransfected LOVO cells and LOVO-pcDNA3 o The expression of VEGF in the △Np73-LOVO was significantly higher than in untransfected LOVO cells(P〈0. 01 ). Conclusion The overexpression of △Np73 promote the proliferation and vessel growth increase the ability of invasion of human colon cancer.
出处 《肿瘤防治研究》 CAS CSCD 北大核心 2008年第5期317-320,共4页 Cancer Research on Prevention and Treatment
关键词 △Np73 大肠癌 侵袭性 凋亡 VEGF △Np73 Human colon cancer Invasiveness Apoptosis VEGF
  • 相关文献

参考文献9

  • 1彭海霞,关明,周林法,孙晨光,陈宇明,钱爱华,王赛玉.p73对结肠癌细胞侵袭性的影响及其机制研究[J].中华消化杂志,2004,24(7):439-441. 被引量:2
  • 2Nakagawa T, Takahashi M, Ozaki T, et al. Autoinhibitory regu-lation of p73 by DeltaNp73 to modulate cell survival and death through a p73-specific target element within the DeltaNp73 promoter [J]. Mol Cel Biol, 2002, 22 (8):2575- 2585.
  • 3Vossio S, Palescandolo E, Pediconi N,et al. DN-p73 is activated after DNA damage in a p53-dependent manner to regulate p53-indueed cell eyelear rest [J]. Oncogene, 2002, 21 (23) : 3796-3803.
  • 4Casciano I, Mazzocco K, Boni L, et al. Expression of DeltaNp73 is a molecular marker for adverse outcome in neuroblastoma patients [J]. Cell Death Differ, 2002, 9 (3) : 246- 251.
  • 5Goldschneider D, Blanc E, Raguenez G, et al. Differential response of p53 targe genes to p73 overexpression in SH-SYSY neuroblastoma cellline [ J ]. Cell Sci, 2004, 117 ( Pt2 ) : 293-301.
  • 6Frasc F, Vella V, Aloisi A, et al. p73 tumor-suppressor activity is impaired in human thyroid cancer [J]. Cancer Res, 2003,63(18) : 5829-5837.
  • 7Drevs J, Laus C, Mendinger M, et al. Antiangiogenesis: current elinieal data and future perspectives[J]. Onkologie, 2002,25(6) :520-527.
  • 8Garkavtsev I, Kozin SV, Chernova O, et al. The candidate tumour suppress or protein ING4 regulates brain tumour growth and angio-genesis [J]. Nature, 2004,428(6980):328- 332.
  • 9ArbiserJ L. Molecular regulation of angiogenesis and umorigenesis by signa ltransduction pathways: evidence of predictable andrepro-ducible patterns of synergy indiverse neoplasms[J]. Semin Cancer Biol, 2004,14(2):81-91.

二级参考文献7

  • 1Kaghad M, Bonnet H, Yang A, et al. Monoallelically expressed gene related to p53 at lp36, a region frequently deleted in neuroblastoma and other human cancers. Cell, 1997, 90:809 819.
  • 2Garkavtsev I, Kozin SV, Chernova O, et al. The candidate tumour suppressor protein ING4 regulates brain tumour growth and angiogenesis. Nature, 2004,428:328-332.
  • 3Arbiser JL. Molecular regulation of angiogenesis and tumorigenesis by signal transduction pathways: evidence of predictable and reproducible patterns of synergy in diverse neoplasms. Semin Cancer Biol,2004,14:81-91.
  • 4Guan M, Peng HX, Yu B, et al. p73 overexpression and angiogenesis in human colorectal carcinoma. Jpn J Clin Oncol, 2003,33: 21 5-220.
  • 5Concin N, Becker K, Slade N, et al. Transdominant DeltaTAp73 isoforms are frequently up-regulated in ovarian cancer. Evidence for their role as epigenetic p53 inhibitors in vivo. Cancer Res, 2004,64: 2449-2460.
  • 6Stiewe T, Tuve S, Peter M, et al. Quantitative TP73 transcript analysis in hepatocellular carcinomas. Clin Cancer Res, 2004, 10:626-633.
  • 7彭海霞,关明,周林法,孙晨光,朱行,苏兵,钱爱华,王赛玉.结肠癌中P73表达与血管生成的关系研究[J].中华消化杂志,2003,23(9):570-571. 被引量:1

共引文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部