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Updated: Apr 29, 2026
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In vitro tRNA Methylation Assay with the Entamoeba histolytica DNA and tRNA Methyltransferase Dnmt2 Ehmeth Enzyme
Published on: October 19, 2010
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[Triptolide affect the methylation status of HL-60cells]
Ruijun Zhang1, Liangming Ma1, Yujin Lu1
1Department of Hematology, the Affiliated Dayi Hospital of Shanxi Medical University, Taiyuan 030001, China.
Zhonghua Xue Ye Xue Za Zhi = Zhonghua Xueyexue Zazhi
|May 27, 2014
Summary
Triptolide (TP) inhibits human promyelocytic leukemia (HL-60) cell proliferation by down-regulating methyltransferase genes, reducing DNA methylation, and promoting apoptosis. This study explores TP
Area of Science:
- Molecular Biology
- Cancer Research
- Epigenetics
Background:
- Human promyelocytic leukemia (HL-60) cells are a model for studying leukemia.
- Aberrant DNA methylation is implicated in cancer development.
- Triptolide (TP) is a compound with potential anti-cancer properties.
Purpose of the Study:
- To investigate the effect of triptolide (TP) on the methylation status of HL-60 cells.
- To explore the preliminary demethylation mechanism of TP in HL-60 cells.
Main Methods:
- HL-60 cells were treated with varying concentrations of TP (3.125-25 nmol/L) for 24 or 48 hours.
- Cell proliferation was assessed using MTT assay.
- Apoptosis, cell cycle, gene expression (DAPK-1, DNMT1, DNMT3B mRNA via RT-PCR), and DNA methylation (LINE-1, DAPK-1 via MSP) were analyzed.
Main Results:
- TP significantly inhibited HL-60 cell proliferation in a time- and dose-dependent manner.
- TP treatment increased early apoptosis rates and altered cell cycle distribution.
- TP downregulated DNMT1 and DNMT3B mRNA expression, decreased LINE-1 and DAPK-1 gene methylation, and increased DAPK-1 mRNA expression.
Conclusions:
- Triptolide (TP) exhibits anti-leukemic effects by modulating DNA methylation.
- TP down-regulates methyltransferase DNMT1/3B, leading to reduced methylation of DAPK-1 and LINE-1 genes.
- This epigenetic modulation promotes DAPK-1 expression and inhibits HL-60 cell growth.
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