期刊文献+

三氧化二砷在体外抑制结肠癌细胞的研究(英文)

A study on arsenic trioxide inhibiting in vitro growth of human colon cancer cells
暂未订购
导出
摘要 目的在体外观察三氧化二砷(As2O3)对结肠癌细胞系HT-29的抑制作用,并探讨其作用机制,为其是否能作为结肠肿瘤的化疗药物提供理论基础。方法将不同浓度As2O3作用于HT-29细胞不同时间后,用MTT检测细胞抑制率,光镜及透射电镜观察细胞形态学和超微结构的变化,通过流式细胞仪及共聚焦显微镜分析凋亡及自噬。结果4.0μmol/L As2O3作用72h可明显抑制HT-29细胞增殖及诱发其凋亡,且抑制率与药物作用时间及浓度成正比。在凋亡早期细胞形态学变化在光镜下可见细胞缩小变圆,在电镜上可见细胞质浓缩、核固缩及自噬溶酶体。4.0μmol/L As2O3作用72h后HT-29细胞凋亡率为25%。结论As2O3能明显抑制结肠癌细胞系HT-29的增殖,其作用机制与引起凋亡及自噬密切相关。 Objective To observe the effect of arsenic trioxide on the proliferation of human colon cancer cells HT-29 in vitro and investigate its mechanism. Methods HT-29 cells (a human colon cancer cell line) were treated with arsenic trioxide in different concentrations. The inhibition on the proliferation of HT-29 cells was estimated by MTT-assay. Morphological changes were observed under light microscope and electron microscope. Apoptosis and autophagy were analyzed by flow cytometer and confocal microscopy. Results When treated with 4.0μmol/L arsenic trioxide for 72h,the proliferation of HT-29 cells was obviously inhibited and the cell underwent conspicuous apoptosis. The inhibition on the proliferation depended on the exposure time and dose. The cells showed morphological changes at the early stage of apoptosis under the light microscope:the shrunk and round cells;condensed cytoplasma and pycnosis nucleus and autophasosomes could be found under the transmission electron microscope. The rate of the apoptotic cells was 25 % after intervention with low concentration of arsenic trioxide (4.0μmol/L) for 72h. Conclusion Arsenic trioxide could significantly inhibit the proliferation of HT-29 cells, and the proliferation inhibition is closely related to cell apoptosis and autophagy.
出处 《哈尔滨医科大学学报》 CAS 北大核心 2007年第5期444-448,共5页 Journal of Harbin Medical University
关键词 结肠癌细胞 三氧化二砷 凋亡 自噬 colon cancer cell arsenic trioxide apoptosis autophagy
  • 相关文献

参考文献10

  • 1Maeda H, Hori S, Ohizumi H, et al. Effective treatment of advanced solid tumors by the combination of arsenic trioxide and L-buthionine-sulfoximine[J]. Cell Death Differ,2004,11(7) :737-746.
  • 2郭化鑫,陈炜,刘连新,张亭栋.三氧化二砷对结肠癌作用的研究近况[J].中国中西医结合消化杂志,2006,14(3):207-209. 被引量:2
  • 3刘琳,邱少敏,赵伟,夏海鸣,秦叔逵,陈惠英.三氧化二砷诱导人类大肠癌细胞凋亡的分子机制[J].世界华人消化杂志,2004,12(7):1550-1554. 被引量:19
  • 4周晋,孟然,关秀茹,李丽敏,杨宝峰.细胞内砷浓度与三氧化二砷治疗敏感性的关系[J].中国药学杂志,2004,39(3):193-195. 被引量:14
  • 5Bursch W. The autophagosomal-lysosomal compartment in programmed cell death[J]. Cell Death Differ, 2001,8 (6):569-581.
  • 6Yorimitsu T, Klionsky DJ. Autophagy: molecular machinery for self-eating[J]. Cell Death Differ, 2005,12(2) : 1542-1552.
  • 7Gozuacik D, Kimchi A. Autophagy as a cell death and tumor suppressor mechanism[J]. Oncogene, 2004,23 (16) : 2891-2906.
  • 8Shimizu S, Kanaseki T, Mizushima N, et al. Role of Bcl-2 family proteins in a non-apoptotic programmed cell death dependent on autophagy genes[J]. Nat Cell Biol, 2004,6(12) : 1221-1228.
  • 9Yu L, Alva A, Su H, et al. Regulation of an ATG7-beclin 1 program of autophagic cell death by caspase-8 [ J ]. Science, 2004,304 (5676) : 1500-1502.
  • 10Lure JJ, Bauer DE, Kong M, et al. Growth factor regulation of autophagy and cell survival in the absence of apoptosis[J]. Cell ,2005,120(2) :237-248.

二级参考文献47

  • 1Wei Wang~1 Shu-Kui Qin~1 Bao-An Chen~2 Hui-Ying Chen~1 1 Chinese PLA Cancer Center,Chinese PLA 81 Hospital,Nanjing 210002,Jiangshu Province,China2 Affliliated Zhongda Hospital of Southeast University Medical College,Nanjing 210087,Jiangsu Province,China.Experimental study on antitumor effect of arsenic trioxide in combination with cisplatin or doxorubicin on hepatocellular carcinoma[J].World Journal of Gastroenterology,2001,7(5):702-705. 被引量:50
  • 2秦叔逵,陈洪,陈惠英,刘文虎,马军,潘其声.三氧化二砷诱导人肝癌细胞株凋亡的初步研究[J].临床肿瘤学杂志,1998,3(2):40-40. 被引量:48
  • 3陈国强,朱军,石学耕,仲豪杰,刘玮,金小龙,唐伟,李秀松,倪建华,熊树民,沈志祥,马军,张鹏,张亭栋,GClaude,陈赛娟,陈竺,王振义.氧化砷诱导早幼粒细胞白血病细胞凋亡及其分子机制的初步研究[J].中华血液学杂志,1997,18(1):25-28. 被引量:106
  • 4[1]Shen ZY, Shen WY, Chen MH, et al. Reactive oxygen species and antioxidants in apoptosis of esophageal cancer cells induced by As2 03[J]. Int J Mol Med, 2003,11(4) :479.
  • 5[2]Alemany M, Levin J. The effeets of arsenic trioxide (As2O3) onhuman megakaryocytic leukemia cell lines. With a comparison of its effects on other cell lineages [ J ]. Leuk Lymphoma, 2000, 38 ( 1-2 ):153.
  • 6[3]Li D, Du C, Lin Y, et al. Inhibition of growth of human nasopharyngeal cancer xenografts in SCID mice by arsenic trioxide [J]. Tumori, 2002,88(6) :522.
  • 7[4]Kitamura K, Minami Y, Yamamoto K, et al. Involvement of CD95independent caspase 8 activation in arsenic trioxide-induced apoptosis[J]. Leukemia, 2000,14(10):1743.
  • 8[5]Ni JH, Chen GQ, Shen ZX, et al. Pharmacokinetics of intravenous arsenic trioxide in the treatment of acute promyelocytic leukemia [J].Chin J Hematol, 1997,18(6) :250.
  • 9[6]Shen Y, Shen ZX, Yan H, et al. Studies on the clinical efficacy and pharmacokinetics of low-dose arsenic trioxide in the treatment of relapsed acute promyelocytic leukemia: a comparison with conventional dosage [J]. Leukemia, 2001,15(5):735.
  • 10LALLEMAND-BREITENBACH V, EBU J, PURION F, et al. Role of Promyelocytic leukemia(PML) Sumolation in nuclear body formation 11s proteasome recruitment and As203-induced PML or PML/retinoic acid receptor alpha degradation[J]. J Exp Med, 2001,193:1361-1371.

共引文献32

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