Tet2-mediated DNA demethylation regulates the proliferation and apoptosis of human leukemia K562 cells

被引:1
|
作者
Qiao, Yan [1 ]
Zhou, Yanhua [1 ]
Yang, Honglan [1 ]
He, Zhixu [1 ,2 ]
Fan, Anran [1 ]
机构
[1] Guizhou Med Univ, Stem Cell & Tissue Engn Res Ctr, Guizhou Prov Key Lab Regenerat Med, Guiyang 550005, Guizhou, Peoples R China
[2] Zunyi Med Univ, Dept Pediat, Affiliated Hosp, Zunyi 563000, Guizhou, Peoples R China
基金
中国国家自然科学基金;
关键词
Tet2; demethylation; proliferation; human leukemia; K562; cells; ACUTE MYELOID-LEUKEMIA; TET PROTEINS; METHYLATION; 5-METHYLCYTOSINE; MLL; 5-HYDROXYMETHYLCYTOSINE; MECHANISM;
D O I
10.14715/cmb/2023.69.3.4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
TET2 is a member of the TET protein family which is responsible for active DNA demethylation through catalyzing the successive oxidation of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC), and mutations of Tet2 frequently lead to hematological malignancies. However, the relationship between Tet2-mediated demethylation and hematological malignancies is unclear. The human leukemia K562 cell line is an immortalized leukemia line that serves as an in vitro model of erythroleukemia. In this study, we investigated the effect of Tet2-mediated demethylation on the apoptosis and proliferation of human leukemia K562 cells and found that knockdown of Tet2 promoted and inhibited K562 cell proliferation and apoptosis, respectively, while upregulation of TET2 enzymatic activity via alpha-ketoglutaric acid (& alpha;-KG) had the opposite effects. Therefore, the Tet2 gene acts as a potential target for the treatment of leukemia, and small molecules that target the Tet2 gene may be used to screen antitumor drugs for hematological malignancies.
引用
收藏
页码:23 / 27
页数:5
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