Effect of decitabine combined with Trichostatin A on MDS cell line SKM-1 in vitro.
- Author:
Li YANG
1
;
Rui-Rong XU
;
Guo-Qi SONG
;
Hong-Ming HANG
;
Hong LIU
;
Sheng-Hua JIANG
;
Xin-Feng WANG
;
Xun-Sheng DING
Author Information
1. Department of Hematology, The Affiliated Hospital, Nantong University, Nantong 226001, Jiangsu Province, China.
- Publication Type:Journal Article
- MeSH:
Antimetabolites, Antineoplastic;
pharmacology;
Apoptosis;
drug effects;
Azacitidine;
analogs & derivatives;
pharmacology;
Cell Differentiation;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Drug Synergism;
Humans;
Hydroxamic Acids;
pharmacology;
Inhibitor of Apoptosis Proteins;
Microtubule-Associated Proteins;
genetics;
metabolism;
Myelodysplastic Syndromes;
pathology;
fas Receptor;
genetics;
metabolism
- From:
Journal of Experimental Hematology
2008;16(4):819-823
- CountryChina
- Language:Chinese
-
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.
