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地西他滨对多发性骨髓瘤U266细胞株生物学行为的影响 被引量:7

Effects of Decitabine on Biological Behavior of U266 Cells
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摘要 本研究以多发性骨髓瘤U266细胞株为实验对象,探讨地西他滨对其生物学功能的影响,为MM的临床治疗提供新思路及实验依据,也为MM的发病机制提供进一步的佐证。应用MTT实验、平板克隆形成试验、FCM分析细胞周期、transw ell迁移及m atrigel侵袭试验分别检测地西他滨对U266细胞增殖、迁移及侵袭能力的影响。结果表明,地西他滨随着浓度增加对U266细胞增殖抑制作用增强,呈剂量和时间依赖性;FCM检测结果表明地西他滨处理后,G0-G1期U266细胞明显增加,S期和G2-M期细胞降低(p<0.05),表明地西他滨可抑制U266细胞DNA合成,将细胞周期阻滞在G0-G1期;低浓度(0.8mm o l/L)地西他滨处理后,U266细胞迁移能力及侵袭力明显降低(p<0.05)。结论:地西他滨对U266细胞的增殖、迁移、侵袭能力均有抑制作用,本研究为地西他滨应用于MM临床治疗提供了一定的实验依据。 This study was aimed to explore the effects of decitabine on the biological behaviour of U266 cells in vitro so as to provide a new thinking and experiment basis, as well as new evidences for the pathogenesis of multiple myeloma. MTT and colony formation assays were used to evaluate the impact of decitabine on the ability of proliferation of U266 cells; flow cytometry was used to analyze the cell distribution in cell cycle; transwell chamber and matrigel assays were used to observe the ability of migration and invasion. The results indicated that decitabine could significantly suppress the proliferation of U266 cells in time- and dose-dependent manners. The flow cytometric analysis demonstrated that the cells in G0- G1 phase significantly increased while the ceils in S and G2/M phase decreased. The migration and matrigel invasing tests showed that the number of cells moving into under chamber of transwell decreased after U266 cells treated with decitabine. It is concluded that decitabine may act as an effective drug for MM by inhibiting the oroliferation, migration and invasion ability, and the specific mechansim needs to be deeply explored.
出处 《中国实验血液学杂志》 CAS CSCD 2011年第4期944-948,共5页 Journal of Experimental Hematology
基金 山西省研究生创新项目(编号20103057) 山西医科大学第二医院青年基金项目(编号20080204)
关键词 多发性骨髓瘤 地西他滨 生物学行为 multiple myeloma decitabine biological behaviour
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参考文献11

  • 1Plimack ER, Kantarjian HM, Issa JP. Decitabine and its role in the treatment of hematopoietic malignancies. Leuk Lymphoma, 2007 ; 48(8) :1472 - 1481.
  • 2佟红艳,林茂芳.5′-杂氮-2′-脱氧胞苷对高危组骨髓增生异常综合征细胞作用的体外研究[J].中国实验血液学杂志,2004,12(4):467-471. 被引量:7
  • 3Braggio E, Maiolino A, Gouveia ME, et al. Methylation status of nine tumor suppressor genes in multiple myeloma. Int J Hematol, 2010;91 ( 1 ) .87 -96.
  • 4Park G, Kang SH, Lee JH, et al. Concurrent p16 methylation pattern as an adverse prognostic factor in multiple myeloma, a methylation-specific polymerase chain reaction study using two different primer sets. Ann Hematol, 2011 ;90( 1 ) :73 -79.
  • 5Walker BA, Wardell CP, Chiecchio L, et al. Aberrant global methylation patterns affect the molecular pathogenesis and prognosis of multiple myeloma. Blood, 2011 ; 117 (2) :553 - 562.
  • 6Yuregir OO, Yurtcu E, Kizilkilic E, et al. Detecting methylation patterns of p16, MGMT, DAPK and E-cadherin genes in multiple myeloma patients. Int J Lab Hematol, 2010; 32(2) :142 -149.
  • 7Heller G, Schmidt WM, Ziegler B, et al. Genome-wide transcriptional response to 5-aza-2'-deoxycytidine and trichostatin a in multiple myeloma cells. Cancer Res ,2008 ;68 ( 1 ) :44 - 54.
  • 8Stewart D J, Issa JP, Kurzrock R, et al. Decitabine effect on tumor global DNA methylation and other parameters in a phase I trial in refractory solid tumors and lymphomas. Clin Cancer Res, 2009;15 (11) :3881 -3888.
  • 9Hollenbach PW, Nguyen AN, Brady H, et al. A comparison of azacitidine and decitabine activities in acute myeloid leukemia cell lines. PLoS One, 2010;5(2) :e9001.
  • 10Lavelle D, DeSimone J, Hankewych M, et al. Decitabine induces cell cycle arrest at the G1 phase via p21 (WAF1) and the G2/M phase via the p38 MAP kinase pathway. Leuk Res, 2003; 27 ( 11 ) :999 - 1007.

二级参考文献9

  • 1Lubbert M, Wijermans P, Kunzmann R, et al. Cytogenetic responses in high-risk myelodysplastic syndrome following low-dose treatment with the DNA methylation inhibitor 5-aza-2'-deoxycytidine. BrJ Haematol. 2001; 114:349-357
  • 2Wijermans P, Lubbert M, Verhoef G, et al. Low-dose 5-aza-2'-deoxycytidine, a DNA hypomethylating agent, for the treatment of high-risk myelodysplastic syndrome: a multicenter phase Ⅱ study in elderly patients. J Clin Oncol, 2000; 18: 956 - 962
  • 3Momparler RL, Bouchard J, Samson J. Induction of differentiation and inhibition of DNA methylation in HL-60 myeloid leukemic cells by 5-aza-2'-deoxycytidine. Leuk Res, 1985; 9:1361 - 1366
  • 4Toyota M, Kopecky KJ, Yoyota MO, et al. Methylation profiling in acute myeloid leukemia. Blood, 2001; 97:2824-2829
  • 5Mizuno S, Chijiwa T, Okamura T, et al. Expression of DNA methyltransferases DNMT1, 3A and 3B in normal hematopoiesis and in acute and chronic myelogenous leukemia. Blood. 2001; 97:1172- 1179
  • 6Herman JG, Civin CI, Issa JP, et al. Distinct patterns of inactivation of p15INK4B and p16INK4A characterize the major types in hematological malignancies. Cancer Res, 1997; 57:837-841
  • 7Sorm F, Vesely J. Effect of 5-aza-2'-deoxycytidine against leukemia and hemopoietic tissues in AKR mice. Neoplasma, 1968; 15:339- 343
  • 8Quesnel B, Guillerm G, Vereecque R, et al. Methylation of the p15(INK4b) gene in myelodysplastic syndromes is frequent and acquired during disease progression. Blood. 1998; 91: 2985 - 2990
  • 9佟红艳,林茂芳.DNA甲基转移酶在骨髓增生异常综合征与白血病细胞中的表达[J].中华血液学杂志,2003,24(6):323-324. 被引量:5

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