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Effect and Comparison of Sodium Butyrate and Trichostatin A on the Proliferation/Differentiation of K562 被引量:1

Effect and Comparison of Sodium Butyrate and Trichostatin A on the Proliferation/Differentiation of K562
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摘要 In order to explore the molecular mechanisms of sodium butyrate and trichostatin A on K562 cell proliferation/differentiation, K562 cells were grown in the absence or presence of sodium butyrate or trichostatin A The percentage of viable cells was determined by trypan blue exclusion Differentiation was determined by nitro-blue tetrazolium (NBT) reduction and cell surface adhesion molecules analyzed by FACS Cell cycle distribution was studied after DNA staining by propidium iodide Cell cycle regulatory proteins were detected by Western blot and reverse transcription-polymerase chain reaction The results showed that sodiun butyrate blocked cells mainly at the G0/G1 phase of the cell cycle, whereas trichostatin A arrested the cells at G2 phase Sodium butyrate could down-regulate the mRNA expression of cyclin D1, but not affect its protein expression; down-regulate the protein expression of cyclin D3, but not affect its mRNA expression Trichostatin A showed similar effects on cyclin D1 and D3 as sodium butyrate Both sodium butyrate and trichostatin A could stimulate p21 expression of K562 cells at mRNA and protein levels It may be concluded that sodium butyrate and trichostatin A could promote the proliferation/differentiation of the K562 cells, which might be contributed to the induced expression of cyclin D3 and p21 proteins In order to explore the molecular mechanisms of sodium butyrate and trichostatin A on K562 cell proliferation/differentiation, K562 cells were grown in the absence or presence of sodium butyrate or trichostatin A The percentage of viable cells was determined by trypan blue exclusion Differentiation was determined by nitro-blue tetrazolium (NBT) reduction and cell surface adhesion molecules analyzed by FACS Cell cycle distribution was studied after DNA staining by propidium iodide Cell cycle regulatory proteins were detected by Western blot and reverse transcription-polymerase chain reaction The results showed that sodiun butyrate blocked cells mainly at the G0/G1 phase of the cell cycle, whereas trichostatin A arrested the cells at G2 phase Sodium butyrate could down-regulate the mRNA expression of cyclin D1, but not affect its protein expression; down-regulate the protein expression of cyclin D3, but not affect its mRNA expression Trichostatin A showed similar effects on cyclin D1 and D3 as sodium butyrate Both sodium butyrate and trichostatin A could stimulate p21 expression of K562 cells at mRNA and protein levels It may be concluded that sodium butyrate and trichostatin A could promote the proliferation/differentiation of the K562 cells, which might be contributed to the induced expression of cyclin D3 and p21 proteins
出处 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2003年第3期249-253,共5页 华中科技大学学报(医学英德文版)
基金 ThisprojectwassupportedbyagrantfromNationalNaturalSciencesFoundationofChina (No 30 0 70 32 6 )
关键词 sodium butyrate cyclin D P21 trichostatin A sodium butyrate cyclin D p21 trichostatin A
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  • 2Hu E D,Chen Z X,Fredrickson T et al.Cloning and characterization of a novel human class I histone deace-tylase that functions as a transcription repressor[].Bio Chem.2000
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  • 4Murata M,Towatari M,Kosugi H et al.Apoptotic cyto-toxic effects of a histone deacetylase inhibitor, FK228, on malignant lymphoid cells[].Japanese Journal of Cancer Research.2000
  • 5Mariadason J M,Corner G A,Augenlicht L H.Genetic reprogramming in pathways of colonic cell maturation induced by short chain fatty acids: comparison with trichostatin A, sulindac, and curcumin and implications for chemoprevention of colon cancer[].Cancer Research.2000
  • 6Yang W M,Tsai S C,Wen Y D et al.Functional domains of histone deacetylase-3[].Biological Chemistry.2002
  • 7Alao J P,Lam E W,Ali S et al.Histone deacetylase inhibitor trichostatin A represses estrogen receptor alpha-dependent transcription and promotes proteasomal degradation of cyclin D1 in human breast carcinoma cell lines[].Clinical Cancer Research.2004
  • 8Chen W,Chen Y,Gu J et al.Effects of curcumin on proliferation of K562 cells involves STAT5 signal transduc-tion pathway[].Chin J Hematol (Chinese).2004
  • 9Kahata K,Hayashi M,Asaka M et al.Regulation of transforming growth factor-beta and bone morphogenetic protein signaling by transcriptional coactivator GCN5[].Genes to Cells Devoted to Molecular Cellular Mechanisms.2004
  • 10Secrist J P,Zhou X,Richon V M.HDAC inhibitors for the treatment of cancer[].Current Opinion in Investigational Drugs.2003

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