Question: What is the mechanism of action of  trichostatin A (TSA) as an antitumoral agent?

Context:
histone deacetylase inhibitor trichostatin A (TSA), an agent that also targets cancer cells and tumor vasculature
Histone deacetylase (HDAC) inhibitors are promising antitumoral drugs.
 trichostatin A and FK901228 showed higher potency
istone deacetylase inhibitors (HDACi) show promise as a novel class of antitumoral agents and have shown the ability to induce apoptosis of tumor cells. 
we conducted a functional gene screen approach named suppression of mortality by antisense rescue technique to identify the key genes responsible for the tumor-selective killing trichostatin A
ydroxamic acid (HA)-based histone deacetylase (HDAC) inhibitors, with trichostatin A (TSA) as the reference compound, are potential antitumoral drugs and show promise in the creation of long-term primary cell cultures
Trichostatin A (TSA), a histone deacetylase inhibitor with promising antifibrotic and antitumoral properties
Trichostatin A (TSA) is a classic histone deacetylases inhibitor (HDACi) that specifically inhibits the biochemical functions of HDAC and is demonstrated to be an active anticancer drug.
Histone deacetylase inhibitors (HDACi) are anticancer agents targeting epigenetic regulation of gene expression
ive MM cell lines were treated with trichostatin A
novel potential anticancer drug histone deacetylase (HDAC) and inhibitor trichostatin A (TSA) 
Histone deacetylase (HDAC) inhibitors represent a promising class of potential anticancer agents for treatment of human malignancies. In this study, we investigated the effect of trichostatin A (TSA), one such HDAC inhibitor
Trichostatin A (TSA) is a potent histone deacetylase inhibitor and widely used as a promising anticancer agent
we found that a histone deacetylase (HDAC) inhibitor, trichostatin A (TSA), inhibited cell proliferation and invasion
e reported a novel potential anticancer strategy by using histone deacetylase (HDAC) inhibitor to enhance the action of endocrine therapy in ERα-positive breast cancer cell. The well-described HDAC inhibitor, trichostatin A (TSA
We determined whether the HDAC inhibitor, Tricostatin A (TSA) in combination with curcumin would produce greater antiproliferative 
trichostatin A (TSA) exert antitumor activity as histone deacetylase inhibitors, 
anticancer activity of anticancer agent trichostatin A (the histone deacetylase inhibitor)
One of the advantages of the use of histone deacetylase inhibitors, such as TSA, is that its effects have been found to be more potent toward cancer cells compared to normal cells.
 the HDAC inhibitor trichostatin A (TSA). However, only combined treatment with TSA/paclitaxel caused synergistic inhibition of cell growth.
a histone deacetylase inhibitor, trichostatin A (TSA), was proven to be a chemo-sensitizer on human erythroleukemia cells
we demonstrated that the HDIs butyrate and trichostatin A (TSA) directly repress c-Src proto-oncogene expression in many cancer cell lines.
istone deacetylase inhibitors (HDIs) induce cell cycle arrest, differentiation and/or apoptosis in numerous cancer cell types
The results suggest that TSA inhibits bladder carcinoma cell growth
istone deacetylase inhibitors (HDACis) are emerging as a promising new class of anticancer agents displaying growth-inhibitory activity and low toxicity in vivo. In this study, we examined the effect of sodium butyrate (NaB) and trichostatin A (TSA
the in vitro effects of HDAC inhibitors, such as trichostatin A (TSA), sodium butyrate, depsipeptide (FR901228, FK228), valproic acid (VPA) and suberoylanilide hydroxamic acid (SAHA), and the demethylating agent, 5-aza-CdR used alone and in combination treatment of human cancer cells

Answer: Trichostatin A (TSA) exerts antitumoral activity as a histone deacetylase inhibitor