cellular response to trichostatin A

Definition

Target type: biologicalprocess

Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a trichostatin A stimulus. [GOC:yaf, PMID:20181743]

Trichostatin A (TSA) is a potent inhibitor of histone deacetylases (HDACs), a family of enzymes that remove acetyl groups from lysine residues on histone proteins. Histone acetylation is a key regulatory mechanism in gene expression, as it affects chromatin structure and accessibility to transcription factors. By inhibiting HDACs, TSA increases histone acetylation levels, leading to a more open chromatin conformation and enhanced gene transcription.

The cellular response to TSA is complex and multifaceted, involving a wide range of molecular and cellular pathways. Some of the key aspects of this response include:

1. **Transcriptional Activation:** TSA induces the expression of a large number of genes, including those involved in cell cycle regulation, differentiation, apoptosis, and stress response. This activation is mediated by the increased acetylation of histones at the promoters of these genes, making them more accessible to transcription factors.
2. **Cell Cycle Regulation:** TSA can arrest cells in different phases of the cell cycle, depending on the cell type and the concentration of TSA. It can induce G1 arrest by inhibiting the expression of cyclins and CDKs that are essential for G1-S transition. In some cases, TSA can also trigger S-phase arrest and G2/M arrest.
3. **Differentiation and Development:** TSA has been shown to promote differentiation in various cell types, including neuronal cells, muscle cells, and hematopoietic cells. This effect is thought to be related to the altered expression of genes involved in cell fate determination and differentiation pathways.
4. **Apoptosis and Cell Death:** TSA can induce apoptosis, or programmed cell death, in some cancer cells. This effect is mediated by the upregulation of pro-apoptotic genes and the downregulation of anti-apoptotic genes.
5. **Stress Response:** TSA can activate stress response pathways, such as the unfolded protein response (UPR), which is triggered by the accumulation of misfolded proteins in the endoplasmic reticulum. This response aims to restore protein homeostasis and protect the cell from damage.
6. **Epigenetic Remodeling:** TSA induces long-lasting changes in gene expression through epigenetic modifications. This includes alterations in histone acetylation patterns, DNA methylation, and chromatin structure, which can be inherited by daughter cells.

Overall, the cellular response to TSA is highly dynamic and depends on various factors, including cell type, concentration of TSA, and the duration of exposure. The profound effects of TSA on gene expression and cellular processes make it a valuable tool for studying epigenetic mechanisms and the role of histone acetylation in cellular function. It also holds therapeutic potential in various diseases, particularly cancer, where its ability to induce differentiation and apoptosis has shown promising results in preclinical studies.'
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Proteins (1)

Compounds (10)