ArticleToxicological sciences : an official journal of the Society of Toxicology2018
Differentially Expressed mRNA Targets of Differentially Expressed miRNAs Predict Changes in the TP53 Axis and Carcinogenesis-Related Pathways in Human Keratinocytes Chronically Exposed to Arsenic.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Deficient arsenic methylation and global proteomic reprogramming in human keratinocytes during arsenic-induced skin carcinogenesis.Archives of toxicology · 2026Article
- Dysregulation of mRNA expression by hsa-miR-186 overexpression in arsenic-induced skin carcinogenesis.Toxicology and applied pharmacology · 2025Article
- Micro RNA Dysregulation in Keratinocyte Carcinomas: Clinical Evidence, Functional Impact, and Future Directions.International journal of molecular sciences · 2024Review
- Arsenic-induced prostate cancer: an enigma.Medical oncology (Northwood, London, England) · 2024Review
- Exploring the intricate relationship between miRNA dysregulation and breast cancer development: insights into the impact of environmental chemicals.Frontiers in immunology · 2024Review
- Arsenic and UVR co-exposure results in unique gene expression profile identifying key co-carcinogenic mechanisms.Toxicology and applied pharmacology · 2024Article
- Article
- Clonal variability in chromosomal instability as a potential driver in the acquisition of tumorigenic phenotype in chronic arsenic-exposed and hsa-miR-186 overexpressing human keratinocytes.Toxicology and applied pharmacology · 2023Article
- miRNAs and arsenic-induced carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Review
- Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Delineating the Effects of Passaging and Exposure in a Longitudinal Study of Arsenic-Induced Squamous Cell Carcinoma in a HaCaT Cell Line Model.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Temporal Modulation of Differential Alternative Splicing in HaCaT Human Keratinocyte Cell Line Chronically Exposed to Arsenic for up to 28 Wk.Environmental health perspectives · 2022Article
- Dysregulation of microRNAs in metal-induced angiogenesis and carcinogenesis.Seminars in cancer biology · 2021Review
- 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
- Arsenic-induced changes in miRNA expression in cancer and other diseases.Toxicology and applied pharmacology · 2020Review
- Inorganic arsenic promotes luminal to basal transition and metastasis of breast cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Sublethal exposure of small few-layer graphene promotes metabolic alterations in human skin cells.Scientific reports · 2020Article
- Arsenite Exposure Displaces Zinc from ZRANB2 Leading to Altered Splicing.Chemical research in toxicology · 2020Article
- NEnvironmental pollution (Barking, Essex : 1987) · 2020Article
- Overexpression of hsa-miR-186 induces chromosomal instability in arsenic-exposed human keratinocytes.Toxicology and applied pharmacology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Arsenic is a widely distributed toxic natural element. Chronic arsenic ingestion causes several cancers, especially skin cancer. Arsenic-induced cancer mechanisms are not well defined, but several studies indicate that mutation is not the driving force and that microRNA expression changes play a role. Chronic low arsenite exposure malignantly transforms immortalized human keratinocytes (HaCaT), serving as a model for arsenic-induced skin carcinogenesis. Early changes in miRNA expression in HaCaT cells chronically exposed to arsenite will reveal early steps in transformation. HaCaT cells were maintained with 0/100 nM NaAsO2 for 3 and 7 weeks. Total RNA was purified. miRNA and mRNA expression was assayed using Affymetrix microarrays. Targets of differentially expressed miRNAs were collected from TargetScan 6.2, intersected with differentially expressed mRNAs using Partek Genomic Suite software, and mapped to their pathways using MetaCore software. MDM2, HMGB1 and TP53 mRNA, and protein levels were assayed by RT-qPCR and Western blot. Numerous miRNAs and mRNAs involved in carcinogenesis pathways in other systems were differentially expressed at 3 and 7 weeks. A TP53 regulatory network including MDM2 and HMGB1 was predicted by the miRNA and mRNA networks. Total TP53 and TP53-S15-phosphorylation were induced. However, TP53-K382-hypoacetylation suggested that the induced TP53 is inactive in arsenic exposed cells. Our data provide strong evidence that early changes in miRNAs and target mRNAs may contribute to arsenic-induced carcinogenesis.
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