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Updated: Jul 2, 2026
Multiomics Analysis of TMEM200A as a Pan-Cancer Biomarker
Published on: September 15, 2023
Gastric cancer cell lines induced by trichostatin A
Xiao-Ming Zou1, Yun-Long Li, Hao Wang
1Department of General Surgery, the Second Clinical College, Harbin Medical University, Harbin 150086, Heilongjiang Province, China.
Aim:
To explore the effect of trichostatin A (TSA) on apoptosis and acetylated histone H3 levels in gastric cancer cell lines BGC-823 and SGC-7901.
Methods:
The effect of TSA on growth inhibition and apoptosis was examined by MTT, fluorescence microscopy and PI single-labeled flow cytometry. The acetylated histone H3 level was detected by Western blot.
Results:
TSA induced apoptosis in gastric cancer cell lines BGC-823 and SGC-7901 was in a dose and time-dependent manner. Apoptotic cells varied significantly between TSA treated groups (37.5 ng/mL 72 h for BGC-823 cell line and 75 ng/mL 72 h for SGC-7901 cell line) and control group (0.85+/-0.14 vs 1.14+/-0.07, P=0.02; 0.94+/-0.07 vs 1.15+/-0.06, P=0.02). Morphologic changes of apoptosis, including nuclear chromatin condensation and fluorescence strength, were observed under fluorescence microscopy. TSA treatment in BGC-823 and SGC-7901 cell lines obviously induced cell apoptosis, which was demonstrated by the increased percentage of sub-G1 phase cells, the reduction of G1-phase cells and the increase of apoptosis rates in flow cytometric analysis. The result of Western blot showed that the expression of acetylated histone H3 increased in BGC-823 and SGC-7901 TSA treatment groups as compared with the control group.
Conclusion:
TSA can induce cell apoptosis in BGC-823 and SGC-7901 cell lines. The expression of acetylated histone H3 might be correlated with apoptosis.
Insights
Trichostatin A (TSA) induces apoptosis in gastric cancer cells BGC-823 and SGC-7901 in a dose- and time-dependent manner. This effect may be linked to increased acetylated histone H3 expression.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Gastric cancer remains a significant global health challenge.
- Understanding the molecular mechanisms of gastric cancer cell death is crucial for developing novel therapies.
- Trichostatin A (TSA) is a known histone deacetylase inhibitor with potential anti-cancer properties.
Purpose of the Study:
- To investigate the impact of Trichostatin A (TSA) on apoptosis in human gastric cancer cell lines.
- To examine the effect of TSA on the levels of acetylated histone H3 in these cell lines.
- To explore the relationship between TSA-induced apoptosis and histone acetylation.
Main Methods:
- Cell viability was assessed using the MTT assay.
- Apoptosis was analyzed via fluorescence microscopy and propidium iodide (PI) staining followed by flow cytometry.
- Western blot was employed to detect changes in acetylated histone H3 expression.
Main Results:
- TSA demonstrated a dose- and time-dependent induction of apoptosis in BGC-823 and SGC-7901 gastric cancer cells.
- Morphological changes indicative of apoptosis, such as chromatin condensation, were observed.
- Flow cytometry confirmed increased apoptosis rates, evidenced by a higher percentage of sub-G1 phase cells and a reduction in G1-phase cells.
- Western blot analysis revealed a significant increase in acetylated histone H3 levels in TSA-treated cells compared to controls.
Conclusions:
- Trichostatin A effectively induces apoptosis in BGC-823 and SGC-7901 gastric cancer cell lines.
- The observed apoptosis induction by TSA may be associated with elevated levels of acetylated histone H3.
- These findings suggest a potential therapeutic role for TSA in gastric cancer treatment through the modulation of histone acetylation and apoptosis.
