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STUDY ON THE RELATIONSHIP OF ARSENIC TRIOXIDE-INDUCED BIOLOGICAL EFFECTS AND DEGRADATION OF PML PROTEINS 被引量:2

STUDY ON THE RELATIONSHIP OF ARSENIC TRIOXIDE INDUCED BIOLOGICAL EFFECTS AND DEGRADATION OF PML PROTEINS
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摘要 Objective: To understand whether arsenic trioxide (As2O3 )-induced biological effects are associated with degradation of PML proteins. Methods Acute promyelocytic leukemia (APL) cell line NB4, acute T-lymphocytic leukemia cell line Jurkat, acute myeloid leukemia cell line U937, and chronic myelocytic leukemia blast crisis cell line K562 were used as in vitro models In different cell lines, the As2O3-induced biological effects were determined by cell growth, cell viability, cell morphology, and flow cytometry assay on sub G1 cell content. The alteration of PML proteins was analyzed by immunofluorescence Results in terms of growth inhibition and apoptosis induction, 1. 0μmol/L As2O3 had different effects on different cell lines. However, degradation of PML proteins occurred in all the cell lines with As2O3 treatment. Conclusion As2O3-indued biological effects may be independent of PML protein-degradation. Objective: To understand whether arsenic trioxide (As2O3 )-induced biological effects are associated with degradation of PML proteins. Methods Acute promyelocytic leukemia (APL) cell line NB4, acute T-lymphocytic leukemia cell line Jurkat, acute myeloid leukemia cell line U937, and chronic myelocytic leukemia blast crisis cell line K562 were used as in vitro models In different cell lines, the As2O3-induced biological effects were determined by cell growth, cell viability, cell morphology, and flow cytometry assay on sub G1 cell content. The alteration of PML proteins was analyzed by immunofluorescence Results in terms of growth inhibition and apoptosis induction, 1. 0μmol/L As2O3 had different effects on different cell lines. However, degradation of PML proteins occurred in all the cell lines with As2O3 treatment. Conclusion As2O3-indued biological effects may be independent of PML protein-degradation.
出处 《Journal of Shanghai Second Medical University(Foreign Language Edition)》 2001年第2期71-74,共4页 上海第二医科大学学报(英文版)
基金 Supported by the National Science Foundation of China(NNSFC)(39970270, 39730270), a NNSFC award for Outstanding Yong Scientist
关键词 arsenic trioxide PML apoptosis arsenic trioxide PML apoptosis
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参考文献8

  • 1Zhu J,Koken MH,Quignon F,et al.Arsenic-induced PMLtargeting onto nuclear bodies: implications for the treament ofacute promyelocytic leukemia[].Proceedings of the National Academy of Sciences of the United States of America.1997
  • 2Zhu J,Shi XG,Chu HY,et al.Effect of retinoic acid isomerson proliferation, differentiation and PML relocation in the APLcell line NB4[].Leukemia.1995
  • 3Koken MH,Daniel MT,Gianni M,et al.Retinoic acid, butnot arsenic trioxide, degrades the PLZF/RARalpha fusion protein, without inducing terminal differentiation or apoptosis, in aRA-therapy resistant t (11; 17 ) (q23; q21 ) APL patient[].Oncegene.1999
  • 4Wang ZG,Rivi R,Delva L,et al.Arsenic trioxide and melarsoprol induce programmed cell death in myeloid leukamia celllines and function in a PML and PML-RARalpha independentmanner[].Blood.1998
  • 5Chen GQ,Shi XG,Tang W,et al.Use of arsenic trioxide(As2O3 ) in the treatment of acute promyelocytic leukemia(APL): 1.As2O3 exerts dose-dependent dual effects on APLcells[].Blood.1997
  • 6Sternsdorf T,Puccetti E,Jensen K,et al.PIG-1/SUMO-1-modified PML-retinoic acid receptor alpha mediates arsenic trioxide-induced apoptosis in acute promyelocytic leukemia[].Molecular and Cellular Biology.1999
  • 7Chen GQ,Zhu J,Shi XG,et al.In vitro studies on cellular andmolecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia: As2O3 induce NB4 cellapoptosis with downregulation of Bcl-2 expression and modulation of PML-RARalpha/PML proteins[].Blood.1996
  • 8Gianni M,Koken MH,Chelbi-Alix MK,et al.Combined arsenic and retinoic acid treatment enhances differentiation andapoptosis in arsenic-resistant NB4 cells[].Blood.1998

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