ArticleEnvironmental health perspectives2006
Exit from arsenite-induced mitotic arrest is p53 dependent.
Article in Environmental health perspectives, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Zinc supplementation prevents mitotic accumulation in human keratinocyte cell lines upon environmentally relevant arsenic exposure.Toxicology and applied pharmacology · 2022Article
- Overexpression of hsa-miR-186 induces chromosomal instability in arsenic-exposed human keratinocytes.Toxicology and applied pharmacology · 2019Article
- Integration of microRNAome, proteomics and metabolomics to analyze arsenic-induced malignant cell transformation.Oncotarget · 2017Article
- Inhibitor of Differentiation/DNA Binding 1 (ID1) Inhibits Etoposide-induced Apoptosis in a c-Jun/c-Fos-dependent Manner.The Journal of biological chemistry · 2016Article
- Disruption of Mitotic Progression by Arsenic.Biological trace element research · 2015Review
- Proteomics-Based Identification of Differentially Abundant Proteins from Human Keratinocytes Exposed to Arsenic Trioxide.Journal of proteomics & bioinformatics · 2014Article
- Cisplatin plus sodium arsenite and hyperthermia induces pseudo-G1 associated apoptotic cell death in ovarian cancer cells.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- The NRF2-mediated oxidative stress response pathway is associated with tumor cell resistance to arsenic trioxide across the NCI-60 panel.BMC medical genomics · 2010Article
- Suppression of p53 and p21CIP1/WAF1 reduces arsenite-induced aneuploidy.Chemical research in toxicology · 2010Article
- Arsenic trioxide suppresses paclitaxel-induced mitotic arrest.Cell proliferation · 2009Article
- Arsenite-induced mitotic death involves stress response and is independent of tubulin polymerization.Toxicology and applied pharmacology · 2008Article
- Subhepatotoxic exposure to arsenic enhances lipopolysaccharide-induced liver injury in mice.Toxicology and applied pharmacology · 2008Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundArsenic is both a human carcinogen and a chemotherapeutic agent, but the mechanism of neither arsenic-induced carcinogenesis nor tumor selective cytotoxicity is clear. Using a model cell line in which p53 expression is regulated exogenously in a tetracycline-off system (TR9-7 cells) , our laboratory has shown that arsenite disrupts mitosis and that p53-deficient cells [p53(-)], in contrast to p53-expressing cells [p53(+)], display greater sensitivity to arsenite-induced mitotic arrest and apoptosis.
objectiveOur goal was to examine the role p53 plays in protecting cells from arsenite-induced mitotic arrest.
methodsp53(+) and p53(-) cells were synchronized in G2 phase using Hoechst 33342 and released from synchrony in the presence or absence of 5 microM sodium arsenite.
resultsMitotic index analysis demonstrated that arsenite treatment delayed exit from G2 in p53(+) and p53(-) cells. Arsenite-treated p53(+) cells exited mitosis normally, whereas p53(-) cells exited mitosis with delayed kinetics. Microarray analysis performed on mRNAs of cells exposed to arsenite for 0 and 3 hr after release from G2 phase synchrony showed that arsenite induced inhibitor of DNA binding-1 (ID1) differentially in p53(+) and p53(-) cells. Immunoblotting confirmed that ID1 induction was more extensive and sustained in p53(+) cells.
conclusionsp53 promotes mitotic exit and leads to more extensive ID1 induction by arsenite. ID1 is a dominant negative inhibitor of transcription that represses cell cycle regulatory genes and is elevated in many tumors. ID1 may play a role in the survival of arsenite-treated p53(+) cells and contribute to arsenic carcinogenicity.
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