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Updated: Feb 8, 2026

An Organotypic High Throughput System for Characterization of Drug Sensitivity of Primary Multiple Myeloma Cells
Published on: July 15, 2015
[Effects of triptolide on the apoptosis and H3K4 protein methylation in multiple myeloma cells]
Cheng-Bo Xu1, Bin Liao1, Jian-Zhen Shen2
1Department of Hematology, The People's Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou 350004.
Objective:
To investigate the effects of triptolide (Chinese Traditional Medicine)on the apoptosis and H3K4 protein methylation in multiple myeloma cells.
Methods:
The RPMI8226 cells were cultured with different concentrations(10,20,40,80 and 160 nmol/L)of triptolide for different incubation time (24 h,48 h and 72 h). The inhibition of triptolide on RPMI8226 cell proliferation was detected by MTT assay. Apoptosis and cell cycle distribution were evaluated by flow cytometry.The expressions of H3K4me2 and trimethylation of histone H3 lysine 4(H3K4me3) in RPMI8226 cells were assayed by Western blot. The changes of expressions of histone methylase SET and MYND domain containing 3(SMYD3) and histone demethylase lysine specific demethylase 1(LSD1) in RPMI8226 cells were verified by qRT-PCR.
Results:
Triptolide had obvious inhibitive effects on proliferation of RPMI8226 cells and showed a dose-and time-dependent manner(P<0.05). Triptolide induced apoptosis and G2/M cell cycle arrest in a dose-dependent manner(P<0.05). Triptolide decreased histone H3K4me2 and H3K4me3 expression in a dose-dependent manner(P<0.05, P<0.01). SMYD3 was significantly depressed at protein expression in a dose-dependent manner(P<0.05), but LSD1 was up-regulated (P<0.05).
Conclusions:
Triptolide could inhibit RPMI8226 cell proliferation,induce the apoptosis and cause G2/M arrest,meanwhile,significantly inhibit the protein expressions of H3K4me2 and H3K4me2 with alter the expression of SMYD3 and LSD1.The effects is probably related to the antitumor mechanism of MM cells induced by triptolide.
Insights
Triptolide, a traditional Chinese medicine, inhibits multiple myeloma cell growth and induces apoptosis. It also reduces H3K4 methylation by altering SMYD3 and LSD1 expression, suggesting an anti-cancer mechanism.
Area of Science:
- Oncology
- Epigenetics
- Pharmacology
Background:
- Multiple myeloma (MM) is a hematological malignancy.
- Understanding novel therapeutic targets is crucial for MM treatment.
- Epigenetic modifications play a role in cancer development.
Purpose of the Study:
- To investigate the effects of triptolide on multiple myeloma cell apoptosis.
- To examine the impact of triptolide on H3K4 protein methylation in MM cells.
- To explore the underlying molecular mechanisms of triptolide's anti-cancer activity.
Main Methods:
- RPMI8226 multiple myeloma cells were treated with varying concentrations of triptolide.
- Cell proliferation was assessed using MTT assay.
- Apoptosis, cell cycle distribution, H3K4me2, H3K4me3, SMYD3, and LSD1 expression were analyzed via flow cytometry and Western blot, qRT-PCR.
Main Results:
- Triptolide significantly inhibited RPMI8226 cell proliferation in a dose- and time-dependent manner.
- Triptolide induced apoptosis and G2/M cell cycle arrest.
- Triptolide decreased H3K4me2 and H3K4me3 levels, downregulated SMYD3, and upregulated LSD1.
Conclusions:
- Triptolide exhibits anti-proliferative and pro-apoptotic effects on multiple myeloma cells.
- Triptolide alters H3K4 methylation by modulating SMYD3 and LSD1 expression.
- These epigenetic changes likely contribute to triptolide's anti-cancer mechanism in multiple myeloma.
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