ArticleCells2022
A Comprehensive Transcriptomic Analysis of Arsenic-Induced Bladder Carcinogenesis.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Arsenic disrupts autophagosome-lysosome fusion in a zinc dependent manner across multiple human skin and lung cells lines.Archives of toxicology · 2026Article
- DNA methylation-mediated silencing of HNF1B promotes bladder cancer progression.Clinical epigenetics · 2026Article
- Dysregulation of mRNA expression by hsa-miR-186 overexpression in arsenic-induced skin carcinogenesis.Toxicology and applied pharmacology · 2025Article
- Association between gestational arsenic exposure and infant physical development: a prospective cohort study.BMC public health · 2024Article
- Arsenic and Human Health: New Molecular Mechanisms For Arsenic-Induced Cancers.Current pollution reports · 2023Article
- Modification of lysine-260 2-hydroxyisobutyrylation destabilizes ALDH1A1 expression to regulate bladder cancer progression.iScience · 2023Article
- Inherited myogenic abilities in muscle precursor cells defined by the mitochondrial complex I-encoding protein.Cell death & disease · 2023Article
- State of the Art of Genomic Technology in Toxicology: A Review.International journal of molecular sciences · 2023Review
- Gene expression profiles to analyze the anticancer and carcinogenic effects of arsenic in bladder cancer.American journal of translational research · 2023Article
- A small molecule inhibitor of Notch1 modulates stemness and suppresses breast cancer cell growth.Frontiers in pharmacology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Arsenic (sodium arsenite: NaAsO2) is a potent carcinogen and a known risk factor for the onset of bladder carcinogenesis. The molecular mechanisms that govern arsenic-induced bladder carcinogenesis remain unclear. We used a physiological concentration of NaAsO2 (250 nM: 33 µg/L) for the malignant transformation of normal bladder epithelial cells (TRT-HU1), exposed for over 12 months. The increased proliferation and colony-forming abilities of arsenic-exposed cells were seen after arsenic exposure from 4 months onwards. Differential gene expression (DEG) analysis revealed that a total of 1558 and 1943 (padj < 0.05) genes were deregulated in 6-month and 12-month arsenic-exposed TRT-HU1 cells. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that cell proliferation and survival pathways, such as the MAPK, PI3K/AKT, and Hippo signaling pathways, were significantly altered. Pathway analysis revealed that the enrichment of stem cell activators such as ALDH1A1, HNF1b, MAL, NR1H4, and CDH1 (p < 0.001) was significantly induced during the transformation compared to respective vehicle controls. Further, these results were validated by qPCR analysis, which corroborated the transcriptomic analysis. Overall, the results suggested that stem cell activators may play a significant role in facilitating the arsenic-exposed cells to gain a survival advantage, enabling the healthy epithelial cells to reprogram into a cancer stem cell phenotype, leading to malignant transformation.
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Registered trials
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