ArticleOncology reports2019
Gene expression and DNA methylation regulation of arsenic in mouse bladder tissues and in human urothelial cells.
Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Metabolic Signature of Arsenic Exposure and Metabolism: The Folic Acid and Creatine Trial.Environmental science & technology · 2025Trial
- Sulfur-Containing Amino Acid Homeostasis in the Central Nervous System: From Physiology Regulation to Metal-Induced Neurotoxicity.Metabolites · 2026Review
- CD73-Overexpressing ADSCs Promote Neurogenic Bladder Repair via A2A-JAK1/STAT3-Mediated Modulation of Inflammation and Macrophage Polarization.Stem cells international · 2026Article
- Toxicogenomics of the Freshwater Oligochaete,International journal of molecular sciences · 2024Article
- Epigenetic regulation of human WIF1 and DNA methylation situation of WIF1 and GSTM5 in urothelial carcinoma.Heliyon · 2023Article
- LncRNA LINC00592 mediates the promoter methylation of WIF1 to promote the development of bladder cancer.Open medicine (Warsaw, Poland) · 2023Article
- Gene expression profiles to analyze the anticancer and carcinogenic effects of arsenic in bladder cancer.American journal of translational research · 2023Article
- Anti-Cancer Effects and Tumor Marker Role of GlutathioneInternational journal of molecular sciences · 2021Article
- Article
- Emerging Biomarkers for Predicting Bladder Cancer Lymph Node Metastasis.Frontiers in oncology · 2021Review
- Serum Proteomic Profiling Analysis of Rats Chronically Exposed to Arsenic.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
According to a report of the International Agency for Research on Cancer, arsenic and inorganic arsenic compounds are classified into Group 1 carcinogens with regard to human health. Epidemiological studies indicate that arsenic is one of the main risk factors for the development of bladder cancer. In the present study, arsenic‑altered gene expression in mouse bladder tissues and in human urothelial cells was compared. In the mouse model, sodium arsenite‑induced mouse urothelial hyperplasia and intracellular inclusions were present. Following DNA array analysis, four genes with differential expression were selected for quantitative real‑time PCR assay. The genes were the following: Cystathionine β‑synthase (CBS), adenosine A1 receptor (ADORA1), metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1) and Wnt inhibitory factor 1 (Wif1). The results indicated a significant increase in the levels of Cbs and Adora1. The analysis of the DNA CpG methylation levels of the mouse Cbs and Adora1 genes revealed no significant change. In contrast to these observations, the four genes were further analyzed in the human normal urothelial cell line SV‑HUC1. The data indicated that WIF1 gene expression was decreased by sodium arsenite, whereas this was not noted for CBS, MALAT1 and ADORA1. Sodium arsenite decreased mRNA and protein expression levels of the WIF1 gene. In addition, the methylation levels of the WIF1 gene were increased. Sodium arsenite inhibited cell proliferation and promoted cell migration as demonstrated in cell functional assays. The gene status was compared in 8 human urothelial cell lines, and WIF1 mRNA expression levels were determined to be higher, whereas DNA CpG methylation levels were lower in SV‑HUC1 cells compared with those noted in the other 7 bladder cancer cell lines. In summary, the data indicated that sodium arsenite decreased WIF1 gene expression and promoted cell migration. The increased methylation levels of WIF1 DNA CpG could be a potential biomarker for bladder cancer.
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