ArticleToxicology and applied pharmacology2017
Cell cycle pathway dysregulation in human keratinocytes during chronic exposure to low arsenite.
Article in Toxicology and applied pharmacology, 2017. 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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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Chronic arsenic exposure and hsa-miR-186 overexpression causes transcriptome-wide differential alternative splicing contributing to skin carcinogenesis in human HaCaT cell line.Archives of toxicology · 2025Article
- DNA damage response inhibition is an early event in cadmium-induced breast carcinogenesis.Toxicology and applied pharmacology · 2025Article
- Dysregulation of mRNA expression by hsa-miR-186 overexpression in arsenic-induced skin carcinogenesis.Toxicology and applied pharmacology · 2025Article
- Article
- Zinc supplementation prevents mitotic accumulation in human keratinocyte cell lines upon environmentally relevant arsenic exposure.Toxicology and applied pharmacology · 2022Article
- A tEMTing target? Clinical and experimental evidence for epithelial-mesenchymal transition in the progression of cutaneous squamous cell carcinoma (a scoping systematic review).Discover oncology · 2022Article
- Dynamic alteration in miRNA and mRNA expression profiles at different stages of chronic arsenic exposure-induced carcinogenesis in a human cell culture model of skin cancer.Archives of toxicology · 2021Article
- Overexpression of hsa-miR-186 induces chromosomal instability in arsenic-exposed human keratinocytes.Toxicology and applied pharmacology · 2019Article
- Akt Regulated Phosphorylation of GSK-3β/Cyclin D1, p21 and p27 Contributes to Cell Proliferation Through Cell Cycle Progression From G1 to S/G2M Phase in Low-Dose Arsenite Exposed HaCat Cells.Frontiers in pharmacology · 2019Article
- miRNA expression profiles of premalignant and malignant arsenic-induced skin lesions.PloS one · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundArsenic is naturally prevalent in the earth's crust and widely distributed in air and water. Chronic low arsenic exposure is associated with several cancers in vivo, including skin cancer, and with transformation in vitro of cell lines including immortalized human keratinocytes (HaCaT). Arsenic also is associated with cell cycle dysregulation at different exposure levels in multiple cell lines. In this work, we analyzed gene expression in HaCaT cells to gain an understanding of gene expression changes contributing to transformation at an early time point.
methodsHaCaT cells were exposed to 0 or 100nM NaAsO
results644 mRNAs were differentially expressed. Cell cycle/cell cycle regulation pathways predominated in the list of dysregulated pathways. Genes involved in replication origin licensing were enriched in the network. Cell cycle assay analysis showed an increase in G2/M compartment in arsenite-exposed cells.
conclusionsArsenite exposure induced differential gene expression indicating dysregulation of cell cycle control, which was confirmed by cell cycle analysis. The results suggest that cell cycle dysregulation is an early event in transformation manifested in cells unable to transit G2/M efficiently. Further study at later time points will reveal additional changes in gene expression related to transformation processes.
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