ArticleBiological trace element research2015
A Potential New Mechanism of Arsenic Carcinogenesis: Depletion of Stem-Loop Binding Protein and Increase in Polyadenylated Canonical Histone H3.1 mRNA.
Article in Biological trace element research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Contribution of histone variants to aneuploidy: a cancer perspective.Frontiers in genetics · 2023Pooled it
- Arsenic exposure and skin cancer: Mechanisms, clinical evidence and public health implications (Review).International journal of molecular medicine · 2026Review
- SATB2 dysregulation generates a novel circular RNA and drives KRAS-like transcriptional reprogramming and transformation-associated phenotypes.Cell communication and signaling : CCS · 2026Article
- LINC00885 promotes lung squamous cell carcinoma by upregulating SLBP expression to activate PI3K/Akt pathway.Clinical and experimental medicine · 2025Article
- Histone supply: a precious commodity for cell identity.The Biochemical journal · 2025Review
- Implications of canonical histone H3.1 and histone variant H3.3 in cancer.Open biology · 2025Review
- Cell signaling and epigenetic regulation of nicotine-induced carcinogenesis.Environmental pollution (Barking, Essex : 1987) · 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
- Epigenomic reprogramming in iAs-mediated carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Polyadenylation of canonical histone H3.1 in 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
- Intermittent fasting induces chronic changes in the hepatic gene expression of Red Jungle Fowl (Gallus gallus).BMC genomics · 2022Article
- Timing of Toenail Collection and Concentrations of Metals in Pancreatic Cancer. Evidence Against Disease Progression Bias.Exposure and health · 2022Article
- Arsenic-induced epigenetic changes in cancer development.Seminars in cancer biology · 2021Review
- Stem-loop binding protein and metal carcinogenesis.Seminars in cancer biology · 2021Review
- Metals and molecular carcinogenesis.Carcinogenesis · 2020Review
- The role of Mediator and Little Elongation Complex in transcription termination.Nature communications · 2020Article
- Histone H2A isoforms: Potential implications in epigenome plasticity and diseases in eukaryotes.Journal of biosciences · 2020Review
- Histone stress: an unexplored source of chromosomal instability in cancer?Current genetics · 2019Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Canonical histones are synthesized with a peak in S-phase, whereas histone variants are formed throughout the cell cycle. Unlike messenger RNA (mRNA) for all other genes with a poly(A) tail, canonical histone mRNAs contain a stem-loop structure at their 3'-ends. This stem-loop structure is the binding site for the stem-loop binding protein (SLBP), a protein involved in canonical histone mRNA processing. Recently, we found that arsenic depletes SLBP by enhancing its proteasomal degradation and epigenetically silencing the promoter of the SLBP gene. The loss of SLBP disrupts histone mRNA processing and induces aberrant polyadenylation of canonical histone H3.1 mRNA. Here, we present new data supporting the idea that the lack of SLBP allows the H3.1 mRNA to be polyadenylated using the downstream poly(A) signal. SLBP was also depleted in arsenic-transformed bronchial epithelial cells (BEAS-2B), which led us to hypothesize the involvement of SLBP and polyadenylated H3.1 mRNA in carcinogenesis. Here, for the first time, we report that overexpression of H3.1 polyadenylated mRNA, and knockdown of SLBP enhances anchorage-independent cell growth. A pcDNA-H3.1 vector with a poly(A) signal sequence was stably transfected into BEAS-2B cells. Polyadenylated H3.1 mRNA and exogenous H3.1 protein levels were significantly increased in cells containing the pcDNA-H3.1 vector. A soft agar assay revealed that cells containing the vector formed significantly higher numbers of colonies compared to wild-type cells. Moreover, small hairpin RNA for SLBP (shSLBP) was used to knockdown the expression of SLBP. Cells stably transfected with the shSLBP vector grew significantly more colonies in soft agar than cells transfected with a control vector. These data suggest that upregulation of polyadenylated H3.1 mRNA holds potential as a mechanism to facilitate carcinogenesis by toxicants such as arsenic that depletes SLBP.
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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.