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Effectiveness of trichostatin A as a potential candidate for anticancer therapy in non-small-cell lung cancer
Nishit K Mukhopadhyay1, Ellen Weisberg, David Gilchrist
1Division of Thoracic Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. nmukhopadhyay@partners.org
Background:
A well-known histone deacetylase inhibitor, trichostatin A, was applied to non-small-cell lung cancer cells to determine whether inhibition of histone deacetylase leads to the production of proteins that either arrest tumor cell growth or lead to tumor cell death.
Methods:
Trichostatin A (0.01 to 1.0 micromol/L) was applied to one normal lung fibroblast and four non-small-cell lung cancer lines, and its effect was determined by flow cytometry, annexin-V staining, immunoprecipitation, and Western blot analysis.
Results:
Trichostatin A demonstrated tenfold greater growth inhibition in all four non-small-cell lung cancer lines compared with normal controls, with a concentration producing 50% inhibition ranging from 0.01 to 0.04 micromol/L for the tumor cell lines and 0.7 micromol/L for the normal lung fibroblast line. Trichostatin A treatment reduced the percentage of cells in S phase (10% to 23%) and increased G1 populations (10% to 40%) as determined by flow cytometry. Both annexin-V binding assay and upregulation of the protein, gelsolin (threefold to tenfold), demonstrated that the tumor cells were apoptotic, whereas normal cells were predominantly in cell cycle arrest. Trichostatin A increased histone H4 acetylation and expression of p21 twofold to 15-fold without significant effect on p16, p27, CDK2, and cyclin D1.
Conclusions:
Collectively, these data suggest that inhibition of histone deacetylation may provide a valuable approach for lung cancer treatment. We evaluated trichostatin A as a potential candidate for anticancer therapy in non-small-cell lung cancer.
Insights
Trichostatin A, a histone deacetylase inhibitor, significantly inhibited non-small-cell lung cancer cell growth and induced apoptosis. This suggests histone deacetylase inhibition is a promising strategy for lung cancer therapy.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Histone deacetylase inhibitors (HDACi) are investigated for cancer therapy.
- Trichostatin A (TSA) is a known HDAC inhibitor.
Purpose of the Study:
- To evaluate TSA's effect on non-small-cell lung cancer (NSCLC) cells.
- To determine if TSA induces tumor cell death or growth arrest.
Main Methods:
- TSA applied to NSCLC lines and normal lung fibroblasts.
- Assessed effects using flow cytometry, annexin-V staining, immunoprecipitation, and Western blot.
Main Results:
- TSA showed tenfold greater growth inhibition in NSCLC cells vs. normal cells.
- TSA induced apoptosis in tumor cells and cell cycle arrest in normal cells.
- TSA increased histone H4 acetylation and p21 expression.
Conclusions:
- Histone deacetylation inhibition is a potential lung cancer treatment strategy.
- TSA demonstrates potential as an anticancer therapeutic for NSCLC.
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