Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.21/3075
Título: Modulation of translation factor's gene expression by histone deacetylase inhibitors in breast cancer cells
Autor: Gonçalves, João
Malta-Vacas, Joana
Louis, Monette
Brault, Laurent
Bagrel, Denyse
Monteiro, Carolino
Brito, Miguel
Palavras-chave: Pharmacology
Antineoplastic agents
Apoptosis
Breast neoplasms
Butyrates
Cell cycle
Enzyme inhibitors
Gene expression regulation
Genes, Neoplasm
Histone deacetylase inhibitors
Hydroxamic acids
Peptide chain elongation, Translational
Protein biosynthesis
Tumor cells, Cultured
Data: Jun-2005
Editora: De Gruyter
Citação: Gonçalves J, Malta-Vacas J, Louis M, Brault L, Bagrel D, Brito M, et al. Modulation of translation factor's gene expression by histone deacetylase inhibitors in breast cancer cells. Clin Chem Lab Med. 2005;43(2):151-6.
Resumo: The histone deacetylase inhibitors sodium butyrate (NaBu) and trichostatin A (TSA) exhibit anti-proliferative activity by causing cell cycle arrest and apoptosis. The mechanisms by which NaBu and TSA cause apoptosis and cell cycle arrest are not yet completely clarified, although these agents are known to modulate the expression of several genes including cell-cycle- and apoptosis-related genes. The enzymes involved in the process of translation have important roles in controlling cell growth and apoptosis, and several of these translation factors have been described as having a causal role in the development of cancer. The expression patterns of the translation mechanism, namely of the elongation factors eEF1A1 and eEF1A2, and of the termination factors eRF1 and eRF3, were studied in the breast cancer cell line MCF-7 by real-time quantitative reverse transcription-polymerase chain reaction after a 24-h treatment with NaBu and TSA. NaBu induced inhibition of translation factors' transcription, whereas TSA caused an increase in mRNA levels. Thus, these two agents may modulate the expression of translation factors through different pathways. We propose that the inhibition caused by NaBu may, in part, be responsible for the cell cycle arrest and apoptosis induced by this agent in MCF-7 cells.
Peer review: yes
URI: http://hdl.handle.net/10400.21/3075
ISSN: 1434-6621
Versão do Editor: http://www.degruyter.com/view/j/cclm.2005.43.issue-2/cclm.2005.025/cclm.2005.025.xml;jsessionid=1F3DC514F909FFB274DFC8C001D8CED7
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