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Published on: August 10, 2017
[Inhibitory effect of trichostatin A on HepG2 cell proliferation and the mechanisms]
Qingqiang Shi1, Guowei Zuo, Ziqiang Feng
1Laboratory of Stem Cell and Tissue Engineering, Department of Histology and Embryology, Chongqing Medical University, Chongqing 400016, China.
Objective:
To investigate the inhibitory effect of trichostatin A (TSA) on the proliferation of HepG2 cells and explore the underlying mechanism.
Methods:
HepG2 cells exposed to different concentrations of TSA for 24, 48, or 72 h were examined for cell growth inhibition using a cell counting kit, changes in cell cycle distribution with flow cytometry, cell apoptosis with annexin V-FTIC/PI double staining, and cell morphology changes under inverted microscope. The expressions of beta-catenin, HDAC1, HDAC3, H3K9, cyclinD1 and Bax proteins in the exposed cells were detected by Western blotting, and the expressions of HDAC1 and HDAC3 mRNAs by quantitative fluorescent PCR.
Results:
Exposure to TSA caused significant dose- and time-dependent inhibition of HepG2 cell proliferation (P<0.05) and resulted in increased cell percentage in G0/G1 and G2/M phases and decreased cell percentage in S phase. The apoptotic index in the control group was (6.22 ± 0.25)%, which increased to (7.17 ± 0.20)% and (18.14 ± 0.42)% after exposure to 250 and 500 nmol/L TSA, respectively. Exposure to 250 and 500 nmol/L TSA also caused cell morphology changes with numerous floating cells. The expressions of beta-catenin, H3K9 and Bax proteins were significantly increased and CyclinD1, HDAC1, and HDAC3 protein expressions decreased in TSA-treated cells, but the expressions of HDAC1 and HDAC3 mRNAs showed no significant changes.
Conclusions:
TSA can inhibit the proliferation of HepG2 cells and induce cell cycle arrest and apoptosis by inhibiting HDAC activity, promoting histone acetylation, and activating Wnt/beta-catenin signaling pathway.
Insights
Trichostatin A (TSA) inhibits HepG2 cell proliferation by inducing cell cycle arrest and apoptosis. This occurs through inhibiting histone deacetylase (HDAC) activity and activating the Wnt/beta-catenin pathway.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- Hepatocellular carcinoma (HCC) remains a significant global health challenge.
- Understanding the molecular mechanisms of HCC proliferation is crucial for developing targeted therapies.
- Trichostatin A (TSA) is a known histone deacetylase (HDAC) inhibitor with potential anti-cancer properties.
Purpose of the Study:
- To investigate the inhibitory effect of trichostatin A (TSA) on HepG2 cell proliferation.
- To elucidate the underlying molecular mechanisms of TSA's action in HepG2 cells.
Main Methods:
- HepG2 cells were treated with varying concentrations of TSA.
- Cell proliferation was assessed using a cell counting kit.
- Cell cycle distribution and apoptosis were analyzed via flow cytometry.
- Protein and mRNA expression levels of key molecules (e.g., beta-catenin, HDACs, cyclin D1, Bax) were determined using Western blotting and qRT-PCR.
Main Results:
- TSA significantly inhibited HepG2 cell proliferation in a dose- and time-dependent manner.
- TSA induced cell cycle arrest at G0/G1 and G2/M phases and increased apoptosis.
- TSA treatment led to increased expression of beta-catenin and Bax, and decreased expression of CyclinD1, HDAC1, and HDAC3 proteins.
Conclusions:
- TSA effectively inhibits HepG2 cell proliferation, induces cell cycle arrest, and promotes apoptosis.
- The mechanism involves inhibition of HDAC activity, increased histone acetylation, and activation of the Wnt/beta-catenin signaling pathway.
- TSA shows promise as a therapeutic agent for hepatocellular carcinoma.
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