ArticleOncogene2003
Inhibition of histone deacetylase activity increases chromosomal instability by the aberrant regulation of mitotic checkpoint activation.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 87 citations in OpenAlex.
- miR-3189-targeted GLUT3 repression by HDAC2 knockdown inhibits glioblastoma tumorigenesis through regulating glucose metabolism and proliferation.Journal of experimental & clinical cancer research : CR · 2022Article
- A new class of cytotoxic agents targets tubulin and disrupts microtubule dynamics.Bioorganic chemistry · 2021Article
- Listening to mother: Long-term maternal effects in mammalian development.Molecular reproduction and development · 2020Review
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- Dietary phytochemical PEITC restricts tumor development via modulation of epigenetic writers and erasers.Scientific reports · 2017Article
- Inhibition of histone deacetylases induces formation of multipolar spindles and subsequent p53-dependent apoptosis in nasopharyngeal carcinoma cells.Oncotarget · 2016Article
- Article
- Post-translational modifications regulate class IIa histone deacetylase (HDAC) function in health and disease.Molecular & cellular proteomics : MCP · 2015Review
- High throughput screening identifies modulators of histone deacetylase inhibitors.BMC genomics · 2014Article
- Targeting histone deacetylases for cancer therapy: from molecular mechanisms to clinical implications.International journal of biological sciences · 2014Review
- Genetic Variations of ABCC2 Gene Associated with Adverse Drug Reactions to Valproic Acid in Korean Epileptic Patients.Genomics & informatics · 2013Article
- The multi zinc-finger protein Trps1 acts as a regulator of histone deacetylation during mitosis.Cell cycle (Georgetown, Tex.) · 2013Article
- Aurora B-dependent regulation of class IIa histone deacetylases by mitotic nuclear localization signal phosphorylation.Molecular & cellular proteomics : MCP · 2012Article
- Cancer-associated alteration of pericentromeric heterochromatin may contribute to chromosome instability.Oncogene · 2012Article
- Hyaluronan suppresses prostate tumor cell proliferation through diminished expression of N-cadherin and aberrant growth factor receptor signaling.Experimental cell research · 2011Article
- Deacetylation and methylation at histone H3 lysine 9 (H3K9) coordinate chromosome condensation during cell cycle progression.Molecules and cells · 2011Article
- Chromatin remodeling, cell proliferation and cell death in valproic acid-treated HeLa cells.PloS one · 2011Article
- O-GlcNAc transferase regulates mitotic chromatin dynamics.The Journal of biological chemistry · 2010Article
- Hyperacetylation in prostate cancer induces cell cycle aberrations, chromatin reorganization and altered gene expression profiles.Journal of cellular and molecular medicine · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone modification through acetylation and deacetylation is a key process in transcription, DNA replication, and chromosome segregation. During mitosis, histones are highly acetylated and chromatin is condensed. Here, we investigate the mechanistic involvement of histone deacetylase (HDAC) activity in the regulation of mitotic checkpoint activation. Inhibition of HDAC activity was found to cause the improper kinetochore localization of the mitotic checkpoint proteins, and to prolong mitotic arrest, and thus to lead to chromosomal instability due to aberrant exit from the mitotic cell cycle arrest. In addition, treatment with HDAC inhibitor attenuated the activations of p38 and ERK kinases, and increased the expression levels of cIAP-1, suggesting that the observed increased adaptation and chromosomal instability induced by inhibiting HDAC activity might be directly connected with the activations of cell survival and/or antiapoptotic signals. Moreover, the treatment of cells with mitotic defects with HDAC inhibitor increased their susceptibility to chromosomal instability. These results support the notion that HDAC activity plays an important role in the regulation of mitotic checkpoint activation, and thus the aberrant control of HDAC activity contributes to chromosomal instability.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.