Gene expression and DNA methylation regulation of arsenic in mouse bladder tissues and in human urothelial cells

Published Jul 20, 2019Oncology reports

How Arsenic Affects Gene Activity and DNA Methylation in Mouse Bladder and Human Urine Tract Cells

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Abstract

Sodium arsenite decreased WIF1 gene expression and promoted cell migration in human urothelial cells.

Arsenic is classified as a Group 1 carcinogen associated with bladder cancer risk.
In mouse bladder tissues, sodium arsenite induced urothelial hyperplasia and intracellular inclusions.
Quantitative analysis revealed significant increases in the expression levels of Cystathionine β-synthase (CBS) and adenosine A1 receptor (ADORA1) genes in response to arsenic.
WIF1 gene expression was significantly decreased by sodium arsenite in human urothelial cells, alongside increased DNA CpG methylation levels.
Sodium arsenite inhibited cell proliferation and promoted migration in functional assays.
WIF1 gene expression was higher and its methylation levels were lower in the SV-HUC1 cell line compared to other bladder cancer cell lines.

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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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Gene expression and DNA methylation regulation of arsenic in mouse bladder tissues and in human urothelial cells

Abstract

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