ArticleScientific reports2017
Upregulation of microRNA-4417 and Its Target Genes Contribute to Nickel Chloride-promoted Lung Epithelial Cell Fibrogenesis and Tumorigenesis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Loss of MEG3 promotes migration and invasion of nickel-transformed cells, partially via upregulation of RUNX2.Toxicology and applied pharmacology · 2026Article
- Review
- Toxic metals in the regulation of epithelial-mesenchymal plasticity: demons or angels?Cancer cell international · 2022Review
- Transcriptional repression of E-cadherin in nickel-exposed lung epithelial cells mediated by loss of Sp1 binding at the promoter.Molecular carcinogenesis · 2022Article
- Epigenetic mechanisms in metal carcinogenesis.Toxicology reports · 2022Review
- Epithelial-mesenchymal transition: Insights into nickel-induced lung diseases.Seminars in cancer biology · 2021Review
- Dysregulation of microRNAs in metal-induced angiogenesis and carcinogenesis.Seminars in cancer biology · 2021Review
- Epimutational effects of electronic cigarettes.Environmental science and pollution research international · 2021Review
- Epithelial to mesenchymal transition and microRNA expression are associated with spindle and apocrine cell morphology in triple-negative breast cancer.Scientific reports · 2021Article
- miR-4417 suppresses keloid fibrosis growth by inhibiting CyclinD1.Journal of biosciences · 2020Article
- Tissue transglutaminase 2 expression is epigenetically regulated in human lung cancer cells and prevents reactive oxygen species-induced apoptosis.Cancer management and research · 2018Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nickel compounds have been classified as carcinogens and shown to be associated with induction of epithelial-mesenchymal transition (EMT) in fibrogenesis and tumorigenesis, as well as the crucial role of microRNAs (miRNAs) and their related genes in controlling EMT and cancer metastasis. Thus, the mechanisms involved in the regulation of EMT in nickel-treated cells are of potential interest in understanding lung fibrosis and tumor progression. We investigated the miRNA-dependent mechanisms involved in nickel-induced EMT in lung epithelial cells. Nickel increased miR-4417 expression and decreased its target gene TAB2 expression. Treatment of cells with TGF-β inhibitor SB525334 significantly blocked NiCl
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Registered trials
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