ArticleToxicological sciences : an official journal of the Society of Toxicology2014
Aberrant microRNA expression likely controls RAS oncogene activation during malignant transformation of human prostate epithelial and stem cells by arsenic.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- A systematic review and meta-analysis of bidirectional effect of arsenic on ERK signaling pathway.Molecular medicine reports · 2018Pooled it
- Endocrine-disrupting chemicals as prostate carcinogens.Nature reviews. Urology · 2025Review
- A systematic review of mechanisms of PTEN gene down-regulation mediated by miRNA in prostate cancer.Heliyon · 2024Article
- circ_0029463 promotes osteoclast differentiation by mediating miR-134-5p/Rab27a axis.Journal of orthopaedic surgery and research · 2024Article
- Arsenic-induced prostate cancer: an enigma.Medical oncology (Northwood, London, England) · 2024Review
- Insights into the complex interactions between Rab22a and extracellular vesicles in cancers.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
- Deregulated microRNAs Involved in Prostate Cancer Aggressiveness and Treatment Resistance Mechanisms.Cancers · 2023Review
- miRNAs and arsenic-induced carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Review
- Dysregulation of microRNAs in metal-induced angiogenesis and carcinogenesis.Seminars in cancer biology · 2021Review
- Advanced bioinformatic analysis and pathway prediction of NSCLC cells upon cisplatin resistance.Scientific reports · 2021Article
- miRNAs as Therapeutic Tools and Biomarkers for Prostate Cancer.Pharmaceutics · 2021Review
- miR-96-5p, miR-134-5p, miR-181b-5p and miR-200b-3p heterogenous expression in sites of prostate cancer versus benign prostate hyperplasia-archival samples study.Histochemistry and cell biology · 2021Article
- Toxic Mechanisms of Five Heavy Metals: Mercury, Lead, Chromium, Cadmium, and Arsenic.Frontiers in pharmacology · 2021Review
- Arsenic-induced changes in miRNA expression in cancer and other diseases.Toxicology and applied pharmacology · 2020Review
- Review
- Transplacental arsenic exposure produced 5-methylcytosine methylation changes and aberrant microRNA expressions in livers of male fetal mice.Toxicology · 2020Article
- Metal carcinogen exposure induces cancer stem cell-like property through epigenetic reprograming: A novel mechanism of metal carcinogenesis.Seminars in cancer biology · 2019Review
- Anti-cancer Effects of a Chemically Modified miR-143 on Bladder Cancer by Either Systemic or Intravesical Treatment.Molecular therapy. Methods & clinical development · 2019Article
- MicroRNA-193b acts as a tumor suppressor in colon cancer progression via targeting RAB22A.Experimental and therapeutic medicine · 2019Article
- MicroRNAs and their role in environmental chemical carcinogenesis.Environmental geochemistry and health · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Inorganic arsenic (iAs), a human carcinogen, potentially targets the prostate. iAs malignantly transforms the RWPE-1 human prostate epithelial line to CAsE-PE cells, and a derivative normal stem cell (SC) line, WPE-stem, to As-Cancer SC (As-CSC) line. MicroRNAs (miRNA) are noncoding but exert negative control on expression by degradation or translational repression of target mRNAs. Aberrant miRNA expression is important in carcinogenesis. A miRNA array of CAsE-PE and As-CSC revealed common altered expression in both for pathways concerning oncogenesis, miRNA biogenesis, cell signaling, proliferation, and tumor metastasis and invasion. The KRAS oncogene is overexpressed in CAsE-PE cells but not by mutation or promoter hypomethylation, and is intensely overexpressed in As-CSC cells. In both transformants, decreased miRNAs targeting KRAS and RAS superfamily members occurred. Reduced miR-134, miR-373, miR-155, miR-138, miR-205, miR-181d, miR-181c, and let-7 in CAsE-PE cells correlated with increased target RAS oncogenes, RAN, RAB27A, RAB22A mRNAs, and KRAS protein. Reduced miR-143, miR-34c-5p, and miR-205 in As-CSC correlated with increased target RAN mRNA, and KRAS, NRAS, and RRAS proteins. The RAS/ERK and PI3K/PTEN/AKT pathways control cell survival, differentiation, and proliferation, and when dysregulated promote a cancer phenotype. iAs transformation increased expression of activated ERK kinase in both transformants and altered components of the PI3K/PTEN/AKT pathway including decreased PTEN and increases in BCL2, BCL-XL, and VEGF in the absence of AKT activation. Thus, dysregulated miRNA expression may be linked to RAS activation in both transformants.
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