期刊文献+
任意字段
题名或关键词
题名
关键词
文摘
作者
第一作者
机构
刊名
分类号
参考文献
作者简介
基金资助
栏目信息

Bmi-1 siRNA对人白血病K562细胞增殖的影响及其机制 被引量：3

RNAi-silenced human Bmi-1 gene inhibits proliferation of human leukemia cell line K562
下载PDF
导出
摘要 目的探讨Bmi-1 siRNA对人白血病K562细胞增殖的影响及其作用机制。方法通过脂质体将化学合成针对Bmi-1基因的siRNA转染K562细胞,采用MTT法观察Bmi-1 siRNA对K562细胞增殖的抑制作用;流式细胞术分析细胞周期变化;Western blot检测Bmi-1siRNA对K562细胞中Bmi-1和P16蛋白表达的影响。结果Bmi-1 siRNA能明显延长K562细胞的倍增时间、G1期比例增加;下调Bmi-1表达的同时上调P16蛋白表达。结论体外化学合成的Bmi-1 siRNA对K562细胞的体外增殖具有明显的抑制作用,下调Bmi-1蛋白表达的同时上调P16蛋白表达。 Objective To explore the silence of B-cell specific Moloney murine leukaemia virus insertion site 1 （ Bmi-1 ） by RNA interference on the proliferation of human leukemia cell line K562 and its mechanisms. Methods Small interfering RNA （siRNA） targeting Bmi-1 gene was designed and double-stranded siRNA was chemically synthesized. After double-stranded siRNA was transfected into K562 cells with Lipofectamine 2000, the proliferation of K562 cells was detected by MTT colorimetry, cell cycle was determined by flow cytometry, and the expression of Bmi-1 and P16 were analyzed by Western blotting. Results The siRNA targeting human Bmi-1 gene effectively prolonged the double time of K562 cells, increased the percentage of cells at G1 phase, and the expression of Bmi-1 was significantly down-regulated but the expression of P16 was up-regulated. Conclusion The siRNA targeting human Bmi-1 gene inhibits the proliferation of K562 cells, and up-regulates the expression of P16 in the cells.
作者 朱勇 胡义德 胡中华
机构地区 第三军医大学新桥医院全军肿瘤诊治研究所
出处 《第三军医大学学报》 CAS CSCD 北大核心 2008年第9期791-794,共4页 Journal of Third Military Medical University
基金 国家自然科学基金(30772144)~~
关键词 BMI-1基因 小分子干扰RNA 人白血病K562细胞 P16蛋白 B-cell specific Moloney murine leukaemia virus insertion site-1 gene small interference RNA human leukemia cell line K562 P16 protein
分类号 R394.3 [医药卫生—医学遗传学] R73-354 [医药卫生—肿瘤]
  • 相关文献

参考文献15

  • 1van-Lohuizen M, Verbeek S, Scheijen B, et al. Identification of cooperating oncogenes in E mu-myc transgenic mice by provirus tagging [J]. Cell, 1991,65(5): 737 -752.
  • 2Jacobs J J, Kieboom K, Marino S, et al. The oncogene and Polycombgroup gene Bmi-1 regulates cell proliferation and senescence through the INK4a locus[J]. Nature, 1999, 397(6715) : 164 -168.
  • 3Grinstein E, Wemet P. Cellular signaling in normal and cancerous stem cells[ J ]. Cell Signal, 2007, 19 (12) : 2428 - 2433.
  • 4Raaphorst F M. Self-renewal of hematopoietic and leukemic stem ceils : a central role for the Polycomb-group gene Bmi-1 [ J]. Trends Immunol, 2003, 24(10): 522-524.
  • 5Kirstetter P, Anderson K, Porse B T, et al. Activation of the canonical Wnt pathway leads to loss of hematopoietic stem cell repopulation and multilineage differentiation block [ J]. Nat Immunol, 2006, 7 (10) : 1048 - 1056.
  • 6Reinisch C, Kandutsch S, Uthman A, et al. Bmi-l: a protein expressed in stem cells, specialized cells and tumors of the gastrointestinal tract[ J]. Histol Histopathol, 2006, 21 ( 11 ) : 1143 - 1149.
  • 7Cui H, Ma J, Ding J, et al. Bmi-1 regulates the differentiation and clonogenic self-renewal of Ⅰ -type neuroblastoma cells in a concentration-dependent manner[ J]. J Biol Chem, 2006, 281 (45): 34696 - 34704.
  • 8Cui H, Hu B, Li T, et al. Bmi-1 is essential for the tumorigenicity of neuroblastoma cells[J]. Am J Pathol, 2007, 170(4) : 1370- 1378.
  • 9Silva J, Garcia V, Garcia J M, et al. Circulating Bmi-1 mRNA as a possible prognostic factor for advanced breast cancer patients [ J ]. Breast Cancer Res, 2007, 9(4) : R55.
  • 10Vonlanthen S, Heighway J, Ahermatt H J, et al. The Bmi-1 oncoprorein is differentially expressed in non-small cell lung cancer and correlates with INK4A-ARF locus expression[ J ]. Br J Cancer, 2001, 84 (10) :1372 1376.

二级参考文献21

  • 1AMBROSINI G,ADIDA C,ALTIERI D C.A novel anti-apoptosis gene,survivin,expressed in cancer and lymphoma[J].Nat Med,1997,3(8):917-921.
  • 2REKER S,BECKER J C,SVANE I M,et al.HLA-B35-restricted immune responses against survivin in cancer patients[J].Int J Cancer,2004,108(6):937 -941.
  • 3SUZUKI A,ITO T,KAWANO H,et al.Survivin initiates procaspase 3/p21 complex formation as a result of interaction with CDK4 to resist Fas-mediated cell death[J].Oncogene,2000,19 (10):1346 -1353.
  • 4KARCZMAREK-BOROWSKA B,FILIP A,WOJCIEROWSKI J,et al.Survivin antiapoptotic gene expression as a prognostic factor in nonsmall cell lung cancer:in situ hybridization study[J].Folia Histochem Cytobiol,2005,43 (4):237-242.
  • 5MONZO M,ROSELL R,FELIP E,et al.A novel anti-apoptosis gene:Re-expression of survivin messenger RNA as a prognosis marker in non-small-cell lung cancers[J].J Clin Oncol,1999,17(7):2100-2104.
  • 6SARELA A I,MACADAM R C,FARMERY S M,et al.Expression of the antiapoptosis gene,survivin,predicts death from recurrent colorectal carcinoma[J].Gut,2000,46(5):645 -650.
  • 7MESRI M,WALL N R,LI J,et al.Cancer gene therapy using a survivin mutant adenovirus[J].J Clin Invest,2001,108 (7):981-990.
  • 8TUTOR O,DIAZ M A,RAMIREZ M,et al.Loss of heterozygosity of p16 correlates with minimal residual disease at the end of the induction therapy in non-high risk childhood B-cell precursor acute lymphoblastic leukemia[J].Leuk Res,2002,26(9):817 -820.
  • 9TOKUGAWA T,SUGIHARA H,TANI T,et al.Modes of silencing of p16 in development of esophageal squamous cell carcinoma[J].Cancer Res,2002,62(17):4938-4944.
  • 10TADA T,WATANABE T,KAZAMA S,et al.Reduced p16 expression correlates with lymphatic invasion in colorectal cancers[J].Hepatogastroenterology,2003,50(54):1756-1760.

共引文献6

同被引文献26

  • 1Vonlanthen S, Helghway J, Tschan M P, et al. Expression of p16INK4a/p16alpha and p19ARF/p16beta is frequently altered in non-small cell lung cancer and correlates with p53 overexpression [ J]. Oncogene, 1998, 17(21 ) : 2779 -2785.
  • 2Bruggeman S W, Hulsman D, Tanger E, et al. Bmi1 controls tumor development in an Inkga/Arf-independent manner in a mouse model for glioma [J]. Cancer Cell, 2007, 12(4): 328-341.
  • 3Park I K, Qian D, Kiel M, et al. Bmi-1 is required for maintenance of aduh self-renewing haematopoietic stem cells [ J]. Nature, 2003, 423 (6937) : 302 -305.
  • 4Becker M, Korn C, Sienerth A R, et al. Polycomb group protein Bmil is required for growth of RAF driven non-small-cell lung cancer [ J].PLoS One, 2009, 4 ( 1 ) : e4230.
  • 5Sangiorgi E, Capecchi M R. Bmil is expressed in vivo in intestinal stem cells[J]. Nat Genet, 2008, 40(7) : 915 -920.
  • 6Vrzalikova K, Skarda J, Ehrmann J, et al. Prognostic value of Bmi-1 oncoprotein expression in NSCLC patients: a tissue mieroarray study [J]. J Cancer Res Clin Oncol, 2008, 134(9) : 1037 -1042.
  • 7Vonlanthen S, Heighway J, Ahennatt H J, et al. The bmi-1 oncoprotein is differentially expressed in non-small cell lung cancer and correlates with INK4A-ARF locus expression[J].Br J Cancer, 2001, 84 (10): 1372 - 1376.
  • 8Natt F. siRNAs in drug discovery: target validation and beyond[J].Curr Opin Mol Ther, 2007, 9(3) : 242 -247.
  • 9Cockrell A S, Kafri T. Gene delivery by lentivirus vectors [ J]. Mol Biotechnol, 2007, 36 (3) : 184 - 204.
  • 10Jacobs J J, Kieboom K, Marino S, et al. The oncogene and Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus[J]. Nature, 1999, 397(6715) : 164 -168.

引证文献3

二级引证文献3

第三军医大学学报
2008年 第9期

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