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Effect of decitabine combined with Trichostatin A on MDS cell line SKM-1 in vitro / 中国实验血液学杂志
Journal of Experimental Hematology ; (6): 819-823, 2008.
Article in Chinese | WPRIM | ID: wpr-267881
ABSTRACT
The study was purposed to explore the effect and mechanisms of decitabine and/or Trichostatin A (TSA) on SKM-1 cells in vitro. The effect of decitabine and/or TSA on proliferation of SKM-1cells was analyzed with trypan blue exclusion; the differentiation of SKM-1 cells was detected by nitro-blue tetrazolium (NBT) reduction and flow cytometry; the apoptosis of cells was measured by Annexin V-FITC; the mRNA expression of Fas, survivin and P15(INK4B) in cells treated with decitabine and/or TSA was evaluated by RT-PCR. The results showed that decitabine and/or TSA were capable of inhibiting SKM-1 cell growth and promoting cell differentiation; they stimulated the expression of CD14 and CD11b and inhibited HLA-DR expression; meanwhile and decitabine or/and TSA could induce cell apoptosis, up-regulate mRNA expression of Fas and P15(INK4B), and down-regulate survivin mRNA expression. It is concluded that decitabine can induce apoptosis/differentiation of SKM-1 cells, whose mechanisms may related to the expression of Fas, survivin and P15(INK4B). Decitabine has the synergistic effect with TSA.
Subject(s)
Full text: Available Index: WPRIM (Western Pacific) Main subject: Pathology / Pharmacology / Azacitidine / Myelodysplastic Syndromes / Cell Differentiation / Apoptosis / Fas Receptor / Cell Line, Tumor / Cell Proliferation / Drug Synergism Limits: Humans Language: Chinese Journal: Journal of Experimental Hematology Year: 2008 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Pathology / Pharmacology / Azacitidine / Myelodysplastic Syndromes / Cell Differentiation / Apoptosis / Fas Receptor / Cell Line, Tumor / Cell Proliferation / Drug Synergism Limits: Humans Language: Chinese Journal: Journal of Experimental Hematology Year: 2008 Type: Article