ArticleGenes & cancer2019
Chronic low dose arsenic exposure preferentially perturbs mitotic phase of the cell cycle.
Article in Genes & cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Heavy Metal-Contaminated Soils and Gastric Cancer Risk: Molecular Insights and the Relevance of a One Health Perspective.International journal of molecular sciences · 2025Review
- 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
- Dysregulation of mRNA expression by hsa-miR-186 overexpression in arsenic-induced skin carcinogenesis.Toxicology and applied pharmacology · 2025Article
- Update of the risk assessment of inorganic arsenic in food.EFSA journal. European Food Safety Authority · 2024Article
- Effect of Long-Term Low-Dose Arsenic Exposure on DNA Methylation and Gene Expression in Human Liver Cells.International journal of molecular sciences · 2023Article
- Somatic loss of the Y chromosome is associated with arsenic exposure among Bangladeshi men.International journal of epidemiology · 2023Article
- miR-186 induces tetraploidy in arsenic exposed human keratinocytes.Ecotoxicology and environmental safety · 2023Article
- Article
- Arsenic(III)-induced oxidative defense and speciation changes in a wild Trametes versicolor strain.PloS one · 2023Article
- Zinc supplementation prevents mitotic accumulation in human keratinocyte cell lines upon environmentally relevant arsenic exposure.Toxicology and applied pharmacology · 2022Article
- The Roles of Histone Post-Translational Modifications in the Formation and Function of a Mitotic Chromosome.International journal of molecular sciences · 2022Review
- Nanoplastics and Arsenic Co-Exposures Exacerbate Oncogenic Biomarkers under an In Vitro Long-Term Exposure Scenario.International journal of molecular sciences · 2022Article
- Arsenic co-carcinogenesis: Inhibition of DNA repair and interaction with zinc finger proteins.Seminars in cancer biology · 2021Review
- Molecular Mechanisms of Arsenic-Induced Disruption of DNA Repair.Chemical research in toxicology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Environmental pollution is a big challenge for human survival. Arsenic compounds are well-known biohazard, the exposure of which is closely linked to onsets of various human diseases, particularly cancers. Upon chronically exposing to arsenic compounds, genomic integrity is often disrupted, leading to tumor development. However, the underlying mechanisms by which chronic, low dose arsenic exposure targets genetic stability to initiate carcinogenesis still remain not fully understood. In this study, human lung epithelial BEAS-2B cells and keratinocytes were treated with 0.5 μM of sodium arsenite for one month (designated as BEAS-2B-SA cells or keratinocytes-SA), and its effect on cell cycle responses was analyzed. After being arrested in mitotic phase of the cell cycle by nocodazole treatment, BEAS-2B-SA cells or keratinocytes-SA were delayed to enter next cytokinesis. The lagging exit of the cells from mitosis was accompanied by a sustained Plk1 phosphorylation, which led to a persistent activation of the mitotic regulators BubR1 and Cdc27. As the result, cyclin B1 (clnB1) degradation was attenuated. BEAS-2B-SA cells or keratinocytes-SA also expressed a constitutively active Akt. The cytogenetic analysis showed an increased numbers of aneuploidy in these cells. The suppression of Akt reversed the aberrant expressions of the mitotic regulators, delay of mitotic exit as well as chromosomal aberrations. Our findings suggest that a long-term exposure to low dose sodium arsenite aberrantly retains the catenation of mitosis, which facilitates establishing genetic instability and predisposes the cells to tumorigenesis.
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