ArticleThe Journal of biological chemistry2014
Arsenic induces polyadenylation of canonical histone mRNA by down-regulating stem-loop-binding protein gene expression.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- Vape-Associated lncRNA Transcript 1 (VALT1) Amplifies the Tumorigenic Effects of e-Cigarette Vapor in Lung Epithelial Cells.Non-coding RNA · 2026Article
- SUMO2 promotes histone pre-mRNA processing by stabilizing histone locus body interactions and facilitating U7 snRNP assembly.Genes & development · 2025Article
- Implications of canonical histone H3.1 and histone variant H3.3 in cancer.Open biology · 2025Review
- Roles of Histone H2B, H3 and H4 Variants in Cancer Development and Prognosis.International journal of molecular sciences · 2024Review
- Characterization of histone chaperone MCM2 as a key regulator in arsenic-induced depletion of H3.3 at genomic loci.Toxicology and applied pharmacology · 2023Article
- An increase in polyadenylation of histone isoforms, Hist1h2ah and Hist2h3c2, is governed by 3'-UTR in de-differentiated and undifferentiated hepatocyte.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Molecular mechanisms of environmental exposures and human disease.Nature reviews. Genetics · 2023Review
- Polyadenylation of canonical histone H3.1 in carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Epigenomic reprogramming in iAs-mediated carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Downregulation of Stem-Loop Binding Protein by Nicotine via α7-Nicotinic Acetylcholine Receptor and Its Role in Nicotine-Induced Cell Transformation.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Stem-loop binding protein and metal carcinogenesis.Seminars in cancer biology · 2021Review
- Arsenic-induced epigenetic changes in cancer development.Seminars in cancer biology · 2021Review
- Article
- Metals and molecular carcinogenesis.Carcinogenesis · 2020Review
- Connections between 3' end processing and DNA damage response: Ten years later.Wiley interdisciplinary reviews. RNA · 2020Review
- The role of Mediator and Little Elongation Complex in transcription termination.Nature communications · 2020Article
- Genomic Tools for Environmental Epigenetics and Implications for Public Health.Current opinion in toxicology · 2019Article
- Histone stress: an unexplored source of chromosomal instability in cancer?Current genetics · 2019Review
- Secretory Expression Fine-Tuning and Directed Evolution of Diacetylchitobiose Deacetylase by Bacillus subtilis.Applied and environmental microbiology · 2019Article
- Nickel and cadmium-induced SLBP depletion: A potential pathway to metal mediated cellular transformation.PloS one · 2017Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
The replication-dependent histone genes are the only metazoan genes whose messenger RNA (mRNA) does not terminate with a poly(A) tail at the 3'-end. Instead, the histone mRNAs display a stem-loop structure at their 3'-end. Stem-loop-binding protein (SLBP) binds the stem-loop and regulates canonical histone mRNA metabolism. Here we report that exposure to arsenic, a carcinogenic metal, decreased cellular levels of SLBP by inducing its proteasomal degradation and inhibiting SLBP transcription via epigenetic mechanisms. Notably, arsenic exposure dramatically increased polyadenylation of canonical histone H3.1 mRNA possibly through down-regulation of SLBP expression. The polyadenylated H3.1 mRNA induced by arsenic was not susceptible to normal degradation that occurs at the end of S phase, resulting in continued presence into mitosis, increased total H3.1 mRNA, and increased H3 protein levels. Excess expression of canonical histones have been shown to increase sensitivity to DNA damage as well as increase the frequency of missing chromosomes and induce genomic instability. Thus, polyadenylation of canonical histone mRNA following arsenic exposure may contribute to arsenic-induced carcinogenesis.
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Registered trials
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.