期刊文献+

高转移肺腺癌细胞系A2和A549中p16表达的研究 被引量:3

Research about the Expression of Tumor Suppressor Gene p16 in Two Lung Adenocarcinoma Cell Lines with High Metastasis Potential:A2 and A549
下载PDF
导出
摘要 [目的]探讨肿瘤抑制基因对肺腺癌细胞生长的抑制作用。[方法]用FuGene转染方法将p16的表达质粒分别转入两个p16未表达的具高转移能力的肺腺癌细胞系A2和A549中 ,并对转染前后的肿瘤细胞进行了细胞生长曲线、凋亡检测、电镜和流式细胞仪分析。[结果]发现A2、A549细胞系转染后的细胞生长曲线的斜率要比转染前低得多 ,电镜分析也可看出转染前后的细胞形态发生了改变 ,但均未检测到凋亡信号。经流式细胞仪分析发现 :转染后的细胞系均在G0~G1 期发生阻滞。[结论]p16基因在A2、A549细胞中表达可以抑制其生长。对于发生了p16基因突变或缺失而导致p16蛋白在数量或功能上发生改变的恶性肿瘤 。 To investigate the suppression effect of tumor suppressor gene in lung adenocarcinoma cells.We transfected wild type p16 gene into two lung adenocarcinoma cell lines with high metastasis potential:A2 and A549.The suppression effects of p16 gene were evaluated by cell growth curve,apoptosis detection,electron microscope detection and flow cytometric analysis.The gradient of cell growth curve of transfected cells was lower than that of the untransfected.Electron microscopy showed the morphologic change in p16 transfected cells.No detectable apoptosis signal was detected in the transfected cells.The result of flow cytometric analysis suggested that there was delay of these cells in G0~G1 phase after p16 gene transfection.[Conclusion]Our results demostrated that expression of p16 gene can suppress the growth of the tumor cells in A2 and A549.
出处 《中国肿瘤》 CAS 2000年第12期574-576,共3页 China Cancer
基金 黑龙江省科学技术计划攻关 青年科学基金资助项目(Q98-9)资助
关键词 P16基因 肺肿瘤 腺癌 基因治疗 p16 gene Lung neoplasms Adenocarcinoma Gene therapy
  • 相关文献

参考文献1

二级参考文献2

  • 1萧枫,中华肿瘤杂志,1996年,18卷,73页
  • 2Zhou P,Oncology,1995年,11卷,571页

共引文献24

同被引文献28

  • 1Olopade OI, Jenkins RB, Ranson DT, et al. Molecular analysis of deletions of the short arm of chromosome 9 in human gliomas. Cancer Res, 1992,53:2523.
  • 2Serrano M, Hanhon GJ, Beach D. A new regulatory motify in cell cycle control specific inhibition of cyclinD/CDK4. Nature, 1993,366:704-707.
  • 3Kamb A, Gruis NA, Weaver-Feldaus J, et al. A cell regulator potentially involved in genesis of many types. Science, 1994,264:436-440.
  • 4Arap W, Nishikawa R, Furnari FB, et al . Replacement of the p16/CDKN2 gene suppresses human glioma cell growth. Cancer Res,1995,55:1351-1354.
  • 5Aytac U, Konishi T, David H, et al. Rb independent inhibition of cell growth by p15INK4B . Biochem Biophys Res commun, 1999,262:534-538.
  • 6Morel AP, Unsal K, Cagatay T, et al. P53 but not p16 INK4A induces growth arrest in retinoblastoma-deficient hepatocellular carcinoma cells. J Hepatol,2000,33:254-265.
  • 7Lukas J,Aagaard L, Strauss M,et al. Oncogenic aberrations of p16 INK4/CDKN2 and cyclin D1 cooperate to deregulate G1 control .Cancer Res, 1996,55 : 1355-1357.
  • 8Sachs Z, Sharpless NE, DePinho RA, et al. p16 (Ink4a) interferes with Abelson virus transformation by enhancing apoptosis. J Virol.2004 ,78:3304-11.
  • 9Kratzke RA. Greatens TM, Rubins TB, et al . RB and p16^INK4a expression in resected non-small cell lung tumors . Cancer Res,1996,56:3415-3420.
  • 10林丽萍,武旗,曹广文.细胞黏附分子CD99与肿瘤关系的研究进展[J].第二军医大学学报,2009,30(3):313-316. 被引量:3

引证文献3

二级引证文献4

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