关键词: 基因, 甲基化诱导静止基因；甲基化；白血病

Abstract: Objective  To explore the association between the methylation degree of TMS1 gene in chronic myeloid leukemia cell line K562 cell and NF-κB. Methods  A total of 6 samples of bone marrow of healthy controls and patients with non-hematologic malignancies were randomly collected as case-control group. Then total RNA was extracted and TMS1 mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR). K562 cells were cultured and treated with decitabine (DCA) with different concentrations. The blank control group and experiment group (0.5μmol/L DCA, 1μmol/L DCA) were set up separately. Methylated degree of TMS1 was detected by methylation specificity polymerase chain reaction (MS-PCR), mRNA and protein of TMS1 and NF-κB in K562 cells were checked by RT-PCR and Western blot, the growth of cells was inspected by CCK-8 and morphologic changes were observed by light microscope. Results  TMS1 mRNA was found in the case-control group, but was absent in K562 cells. The TMS1 gene was exhaustively methylated in the blank control group. After promoter demethylation of TMS1, the expression of NF-κB significantly decreased (P<0.05). The K562 cell proliferation was inhibited in a dose- and time-dependent manner. Conclusion  TMS1 gene presents exhaustive methylation in K562 cells and its silent expression may abnormally activate NF-κB signaling pathway and plays a role in the pathogenesis of leukemia.

Key words: Leukemia, Methylation, Gene, TMS1 gene;