期刊文献+

NPM1突变基因表达抑制K562白血病细胞体外增殖和侵袭 被引量:2

NPM1 Mutations in K562 Cells Inhibits Cell Proliferation and Invasion in Vitro
原文传递
导出
摘要 核仁磷酸蛋白(nucleophosmin,NPM1)突变是近年发现的在急性髓系白血病中发挥重要作用的基因改变,为探讨NPM1突变对K562白血病细胞体外增殖和侵袭能力的影响,将载体pEGFPC1-NPM1-mA转染K562细胞系,构建稳定表达NPM1突变蛋白的白血病细胞株(K562-mA)。利用细胞生长曲线观察细胞体外增殖能力;流式细胞仪检测细胞周期进程改变;细胞粘附、Transwell实验分别用以观察细胞体外粘附、迁移及侵袭能力。结果发现,NPM1突变转染后K562细胞体外增殖能力明显减弱;同时G1期细胞比例明显增高,S期细胞比例显著减低。与未处理组和空载体转染组细胞相比,K562-mA细胞体外迁移能力有所增加,但细胞粘附及侵袭能力却明显减弱。提示NPM1突变基因的表达能够抑制白血病细胞体外增殖和侵袭能力,为进一步深入探讨NPM1突变在白血病发生发展中的调控机制奠定了良好的基础。 Nucleophosmin(NPM1)mutations,described recently,play an important role in acute myeloid leukemia.To investigate the role of NPM1 mutations in K562 leukemic cell proliferation and invasion in vitro,the pEGFPC1-NPM1-mA plasmid vector with NPM1 mutation A(NPM1-mA)was transfected into K562 cells,and the K562-mA cells with stably expressed NPM1-mA protein were established.Cell growth curve was used to determine the proliferation potential in vitro.FCM was used to detect the cell cycle.Cell adhesion assay and Transwell were used to detect the adhesion,migration and invasion capability.The results showed that the proliferation potential of K562-mA cells was decreased.Compared with control groups,the percentage of cells in the G1 phase was increased remarkably and that in the S phase was decreased significantly.In addition,the migration ability of K562-mA cells was enhanced,but the adhesion and invasion capability of cells were attenuated.NPM1 mutations may inhibit K562 cells proliferation and invasion in vitro,which provide a better foundation for studying the molecule mechanisms of NPM1 mutations in leukemiagenesis.
出处 《中国生物工程杂志》 CAS CSCD 北大核心 2010年第11期6-10,共5页 China Biotechnology
基金 国家自然科学基金(30872418) 重庆市科委自然科学基金(CSTC 2010BB5363)资助项目
关键词 白血病 核仁磷酸蛋白 突变 细胞增殖 细胞侵袭 Leukemia Nucleophosmin Mutations Cell proliferation Cell invasion
  • 相关文献

参考文献11

  • 1Falini B, Bolli N, Liso A, et al. Altered nucleophosmin transport in acute myeloid leukaemia with mutated NPM1 ; molecular basis and clinical implications. Leukemia, 2009, 23 ( 10 ) : 1731- 1743.
  • 2Meani N, Alcalay M. Role of nucleophosmin in acute myeloid leukemia. Expert Rev Anticancer Ther, 2009, 9 ( 9 ) : 1283- 1294.
  • 3Zhang Y, Zhang M, Yang L, et al. NPM1 mutations in myelodysplastic syndromes and acute myeloid leukemia with normal karyotype. Leukemia Research, 2007, 31 ( 1 ) : 109-111.
  • 4Piccaluga P P, Sabattini E, Bacci F, et al. Cytoplasmic mutated nucleophosmin (NPM1) in blast crisis of chronic myeloid leukaemia. Leukemia, 2009, 23 (7) : 1370- 1371.
  • 5Cheng K, Grisendi S, Clohessy J G, et al. The leukemiaassociated cytoplasmic nucleophosmin mutant is an oncogene with paradoxical functions: Arf inactivation and induction of cellular senescence. Oncogene, 2007, 26(53):7391-7400.
  • 6den Besten W, Kuo M L, Williams R T, et al. Myeloid Leukemia-Associated Nucleophosmin Mutants Perturb p53- Dependent and Independent Activities of the Arf Tumor Suppressor Protein. Cell Cycle, 2005, 4( 11 ) : 1593-1598.
  • 7Bonetti P, Davoli T, Sironi C, et al. Nucleophosmin and its AML-associated mutant regulate c-Myc turnover through Fbw7γ. J Cell Biol, 2008, 182(1) : 19-26.
  • 8Falini B, Nicoletti I, Martelli M F, et al. Acute myeloid leukemia carrying cytoplasmic/mutated nucleophosmin ( NPMc + AML) : biologic and clinical features. Blood, 2007, 109 ( 3 ) : 874-885.
  • 9Schneider F, Hoster E, Unterhalt M, et al. NPM1 but not FLT3- ITD mutations predict early blast cell clearance and CR rate in patients with normal karyotype AML (NK-AML) or high-risk myelodysplastic syndrome (MDS). Blood, 2009, 113 (21) : 5250-5253.
  • 10Falini B, Mecucci C, Tiacci E,et al. Cytoplasmic Nucleophosmin in Acute Myelogenous Leukemia with a Normal Karyotype. N Engl J Med, 2005, 352(3) : 254- 266.

同被引文献23

  • 1李晟,陈子兴,王玮,岑建农,傅建新,姚利.CXCR4在急性白血病细胞中的表达及其对髓外浸润的意义[J].中华血液学杂志,2004,25(7):405-408. 被引量:15
  • 2宋琳,张志谦.MMP-9信号肽高效诱导PEX重组蛋白在COS7细胞中分泌表达[J].中国生物工程杂志,2007,27(5):1-5. 被引量:3
  • 3Alfano R W, Leppla S H, Liu S H, et al. Inhibition of tumor angiogenesis by the matrix metalloproteinase- activated anthrax lethal toxin in an orthotopic model of anaplastic thyroid Mol Cancer Ther, 2010,9 ( 1 ) : 190 -201.
  • 4Brooks P C, Silletti S, Schalscha T L, et al. Disruption of angiogenesis by PEX, a noncatalytic metalloproteinase fragment with integrin binding activity. Cell, 1998, 92(3) : 391 400.
  • 5Yoshifumi I, Akiko T, Noriko I, et al. Homophilic complex formation of MT1 -MMP facilitates proMMP-2 activation on the cell surface and promotes tumor cell invasion. EMBO J, 2001, 20 (17) : 4782-4793.
  • 6Seung-K K, Theresa G, Cargioli, et al. PEX-producing human neural stem cells inhibit tumor growth in a mouse glioma model. Clin Cancer Res, 2005,11(16) : 5965-5970.
  • 7Song L, Zhang Z Q. China Biotechnology, 2007, 27 (5) : 1-5.
  • 8Watanabe J, Endo Y, Shimada N, et al. Antiangiogenic activity of TZT-1027 (Soblidotin) on chick chorioallantoic membrane and human umbilical vein endothelial cells. In Vivo, 2007, 21 (2) : 297 -304.
  • 9Shao H Y, Miao Z Y, Qin F X, et al. China Biotechnology, 2010, 30(11) :6-10.
  • 10Bobek V, Plachy J, Pinterova D, et al. Development of a green fluorescent protein metastatic-cancer chick-embryo drug-screen model. Clin Exp Metastasis. 2004, 21 ( 4 ) :347 -352.

引证文献2

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