ArticleBMC genomics2015
Inorganic Arsenic-induced cellular transformation is coupled with genome wide changes in chromatin structure, transcriptome and splicing patterns.
Article in BMC genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- 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
- Synergic effect of arsenic exposure related methylation changes in three cohorts exposed to levels of this toxicant.International archives of occupational and environmental health · 2025Article
- Chemoproteomic Approach for Identifying Nuclear Arsenite-Binding Proteins.Chemical research in toxicology · 2025Article
- Sex-specific transcriptomic effects of low-dose inorganic arsenic exposure on bone marrow-derived macrophages.Toxicology · 2025Article
- Unveiling the link between arsenic toxicity and diabetes: an in silico exploration into the role of transcription factors.Toxicological research · 2024Article
- Identification of Sweetness Preference-Related Single-Nucleotide Polymorphisms for Polygenic Risk Scores Associated with Obesity.Nutrients · 2024Article
- Multi-omics analysis reveals the dynamic interplay between Vero host chromatin structure and function during vaccinia virus infection.Communications biology · 2024Article
- A dynamic model of inorganic arsenic-induced carcinogenesis reveals an epigenetic mechanism for epithelial-mesenchymal plasticity.Environmental pollution (Barking, Essex : 1987) · 2024Article
- Unraveling the genetics of arsenic toxicity with cellular morphology QTL.PLoS genetics · 2024Article
- Cell morphology QTL reveal gene by environment interactions in a genetically diverse cell population.bioRxiv : the preprint server for biology · 2023Article
- Effect of Long-Term Low-Dose Arsenic Exposure on DNA Methylation and Gene Expression in Human Liver Cells.International journal of molecular sciences · 2023Article
- Pan-transcriptomic Profiling Demarcates Serendipita Indica-Phosphorus Mediated Tolerance Mechanisms in Rice Exposed to Arsenic Toxicity.Rice (New York, N.Y.) · 2023Article
- Nephroprotective Effects of Selenium Nanoparticles Against Sodium Arsenite-Induced Damages.International journal of nanomedicine · 2023Article
- Epigenomic reprogramming in iAs-mediated carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Epigenetic mechanisms in metal carcinogenesis.Toxicology reports · 2022Review
- Temporal Modulation of Differential Alternative Splicing in HaCaT Human Keratinocyte Cell Line Chronically Exposed to Arsenic for up to 28 Wk.Environmental health perspectives · 2022Article
- Arsenic-induced epigenetic changes in cancer development.Seminars in cancer biology · 2021Review
- Origins, fate, and actions of methylated trivalent metabolites of inorganic arsenic: progress and prospects.Archives of toxicology · 2021Review
- Arsenic-induced changes in miRNA expression in cancer and other diseases.Toxicology and applied pharmacology · 2020Review
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
Abstract
backgroundArsenic (As) exposure is a significant worldwide environmental health concern. Low dose, chronic arsenic exposure has been associated with a higher than normal risk of skin, lung, and bladder cancer, as well as cardiovascular disease and diabetes. While arsenic-induced biological changes play a role in disease pathology, little is known about the dynamic cellular changes resulting from arsenic exposure and withdrawal.
resultsIn these studies, we sought to understand the molecular mechanisms behind the biological changes induced by arsenic exposure. A comprehensive global approach was employed to determine genome-wide changes to chromatin structure, transcriptome patterns and splicing patterns in response to chronic low dose arsenic and its subsequent withdrawal. Our results show that cells exposed to chronic low doses of sodium arsenite have distinct temporal and coordinated chromatin, gene expression, and miRNA changes consistent with differentiation and activation of multiple biochemical pathways. Most of these temporal patterns in gene expression are reversed when arsenic is withdrawn. However, some gene expression patterns remained altered, plausibly as a result of an adaptive response by cells. Additionally, the correlation of changes to gene expression and chromatin structure solidify the role of chromatin structure in gene regulatory changes due to arsenite exposure. Lastly, we show that arsenite exposure influences gene regulation both at the initiation of transcription as well as at the level of splicing.
conclusionsOur results show that adaptation of cells to iAs-mediated EMT is coupled to changes in chromatin structure effecting differential transcriptional and splicing patterns of genes. These studies provide new insights into the mechanism of iAs-mediated pathology, which includes epigenetic chromatin changes coupled with changes to the transcriptome and splicing patterns of key genes.
Indexed as
Identifiers
What OpenQuestion holds
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.