ArticleCancer prevention research (Philadelphia, Pa.)2015
Involvement of epigenetics and EMT-related miRNA in arsenic-induced neoplastic transformation and their potential clinical use.
Article in Cancer prevention research (Philadelphia, Pa.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 55 citations in OpenAlex.
- Arsenic in Drinking Water and Diabetes.Water · 2023Article
- In Vitro Approaches to Determine the Potential Carcinogenic Risk of Environmental Pollutants.International journal of molecular sciences · 2023Review
- miRNAs and arsenic-induced carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Review
- Epigenomic reprogramming in iAs-mediated carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- MicroRNA-Gene Interactions Impacted by Toxic Metal(oid)s during EMT and Carcinogenesis.Cancers · 2022Review
- Biological implications and clinical potential of invasion and migration related miRNAs in glioma.Frontiers in integrative neuroscience · 2022Review
- Arsenic-induced epigenetic changes in cancer development.Seminars in cancer biology · 2021Review
- Dysregulation of microRNAs in metal-induced angiogenesis and carcinogenesis.Seminars in cancer biology · 2021Review
- Arsenic-induced changes in miRNA expression in cancer and other diseases.Toxicology and applied pharmacology · 2020Review
- Metals and molecular carcinogenesis.Carcinogenesis · 2020Review
- Urinary MicroRNAs as Potential Markers for Non-Invasive Diagnosis of Bladder Cancer.International journal of molecular sciences · 2020Article
- Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development.Cells · 2020Review
- Metal carcinogen exposure induces cancer stem cell-like property through epigenetic reprograming: A novel mechanism of metal carcinogenesis.Seminars in cancer biology · 2019Review
- MiR-218-5p targets LHFPL3 to regulate proliferation, migration, and epithelial-mesenchymal transitions of human glioma cells.Bioscience reports · 2019Article
- Epigenetic Alterations in Bladder Cancer.Current urology reports · 2018Review
- Arsenic-Induced Carcinogenesis: The Impact of miRNA Dysregulation.Toxicological sciences : an official journal of the Society of Toxicology · 2018Review
- Malignant Transformation of Human Bronchial Epithelial Cells Induced by Arsenic through STAT3/miR-301a/SMAD4 Loop.Scientific reports · 2018Article
- PI3K/Akt/mTOR Signaling Pathway and the Biphasic Effect of Arsenic in Carcinogenesis.Molecular pharmacology · 2018Review
- Arsenic promotes the COX2/PGE2-SOX2 axis to increase the malignant stemness properties of urothelial cells.International journal of cancer · 2018Article
- Increased O-GlcNAcylation of SNAP29 Drives Arsenic-Induced Autophagic Dysfunction.Molecular and cellular biology · 2018Article
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
Exposure to toxicants leads to cumulative molecular changes that overtime increase a subject's risk of developing urothelial carcinoma. To assess the impact of arsenic exposure at a time progressive manner, we developed and characterized a cell culture model and tested a panel of miRNAs in urine samples from arsenic-exposed subjects, urothelial carcinoma patients, and controls. To prepare an in vitro model, we chronically exposed an immortalized normal human bladder cell line (HUC1) to arsenic. Growth of the HUC1 cells was increased in a time-dependent manner after arsenic treatment and cellular morphology was changed. In a soft agar assay, colonies were observed only in arsenic-treated cells, and the number of colonies gradually increased with longer periods of treatment. Similarly, invaded cells in an invasion assay were observed only in arsenic-treated cells. Withdrawal of arsenic treatment for 2.5 months did not reverse the tumorigenic properties of arsenic-treated cells. Western blot analysis demonstrated decreased PTEN and increased AKT and mTOR in arsenic-treated HUC1 cells. Levels of miR-200a, miR-200b, and miR-200c were downregulated in arsenic-exposed HUC1 cells by quantitative RT-PCR. Furthermore, in human urine, miR-200c and miR-205 were inversely associated with arsenic exposure (P = 0.005 and 0.009, respectively). Expression of miR-205 discriminated cancer cases from controls with high sensitivity and specificity (AUC = 0.845). Our study suggests that exposure to arsenic rapidly induces a multifaceted dedifferentiation program and miR-205 has potential to be used as a marker of arsenic exposure as well as a maker of early urothelial carcinoma detection.
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