ArticleJournal of cellular and molecular medicine2010
Hyperacetylation in prostate cancer induces cell cycle aberrations, chromatin reorganization and altered gene expression profiles.
Article in Journal of cellular and molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Quantification of calreticulin redistribution in LNCaP prostate cancer cells using a fixed-cell imaging workflow.microPublication biology · 2026Article
- Trichostatin A inhibits proliferation of PC3 prostate cancer cells by disrupting the EGFR pathway.Oncology letters · 2019Article
- Nuclear morphometry, epigenetic changes, and clinical relevance in prostate cancer.Advances in experimental medicine and biology · 2014Article
- Targeting inhibitor 2 of protein phosphatase 2A as a therapeutic strategy for prostate cancer treatment.Cancer biology & therapy · 2013Article
- The effects of a histone deacetylase inhibitor on biological behavior of diffuse large B-cell lymphoma cell lines and insights into the underlying mechanisms.Cancer cell international · 2013Article
- Epigenetically induced changes in nuclear textural patterns and gelatinase expression in human fibrosarcoma cells.Cell proliferation · 2013Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone acetylation is a fundamental mechanism in the regulation of local chromatin conformation and gene expression. Research has focused on the impact of altered epigenetic environments on the expression of specific genes and their pathways. However, changes in histone acetylation also have a global impact on the cell. In this study we used digital texture analysis to assess global chromatin patterns following treatment with trichostatin A (TSA) and have observed significant alterations in the condensation and distribution of higher-order chromatin, which were associated with altered gene expression profiles in both immortalised normal PNT1A prostate cell line and androgen-dependent prostate cancer cell line LNCaP. Furthermore, the extent of TSA-induced disruption was both cell cycle and cell line dependent. This was illustrated by the identification of sub-populations of prostate cancer cells expressing high levels of H3K9 acetylation in the G(2)/M phase of the cell cycle that were absent in normal cell populations. In addition, the analysis of enriched populations of G(1) cells showed a global decondensation of chromatin exclusively in normal cells.
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Registered trials
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