ArticleOncotarget2015
Exposure to airborne PM2.5 suppresses microRNA expression and deregulates target oncogenes that cause neoplastic transformation in NIH3T3 cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The trial behind it
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
32 citing papers in PubMed, 54 citations in OpenAlex.
- Corneal biomechanical cues mediated by PAI-2: the origin of PM2.5-induced corneal disease.EMBO molecular medicine · 2026Article
- Synergistic effects ofFrontiers in nutrition · 2026Article
- Molecular mechanisms of air pollution-induced carcinogenesis and the emerging role of microplastics.Human genomics · 2025Review
- Global impact of air pollution on cancer: causal evidence and health inequities across regions from 1990 to 2021.BMC cancer · 2025Article
- Population Cohort-Validated PMToxics · 2025Article
- Epigenetic Clocks in Skin Aging: From Exposome Drivers to Biomarkers and Therapeutic Interventions.Clinical, cosmetic and investigational dermatology · 2025Review
- Air Pollution in Cardio-Oncology and Unraveling the Environmental Nexus:JACC. CardioOncology · 2024Review
- The biological interplay between air pollutants and miRNAs regulation in cancer.Frontiers in cell and developmental biology · 2024Review
- Review
- Article
- Epigenetic mechanisms of particulate matter exposure: air pollution and hazards on human health.Frontiers in genetics · 2023Review
- A comprehensive understanding of ambient particulate matter and its components on the adverse health effects based from epidemiological and laboratory evidence.Particle and fibre toxicology · 2022Review
- Nicotinamide Mononucleotide and Coenzyme Q10 Protects Fibroblast Senescence Induced by Particulate Matter Preconditioned Mast Cells.International journal of molecular sciences · 2022Article
- Reply to BuiAmerican journal of respiratory and critical care medicine · 2022Article
- The Correlation of PM2.5 Exposure with Acute Attack and Steroid Sensitivity in Asthma.BioMed research international · 2022Review
- MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous nephropathy.Frontiers in pharmacology · 2022Article
- Genomic Approach to the Assessment of Adverse Effects of Particulate Matters on Skin Cancer and Other Disorders and Underlying Molecular Mechanisms.Journal of cancer prevention · 2021Review
- Airway hyperresponsiveness development and the toxicity of PM2.5.Environmental science and pollution research international · 2021Review
- Outdoor air pollution and cancer: An overview of the current evidence and public health recommendations.CA: a cancer journal for clinicians · 2020Review
- The SIRT2-mediated deacetylation of AKR1C1 is required for suppressing its pro-metastasis function in Non-Small Cell Lung Cancer.Theranostics · 2020Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term exposure to airborne PM2.5 is associated with increased lung cancer risk but the underlying mechanism remains unclear. We characterized global microRNA and mRNA expression in human bronchial epithelial cells exposed to PM2.5 organic extract and integrally analyzed microRNA-mRNA interactions. Foci formation and xenograft tumorigenesis in mice with NIH3T3 cells expressing genes targeted by microRNAs were performed to explore the oncogenic potential of these genes. We also detected plasma levels of candidate microRNAs in subjects exposed to different levels of air PM2.5 and examined the aberrant expression of genes targeted by these microRNAs in human lung cancer. Under our experimental conditions, treatment of cells with PM2.5 extract resulted in downregulation of 138 microRNAs and aberrant expression of 13 mRNAs (11 upregulation and 2 downregulation). In silico and biochemical analyses suggested SLC30A1, SERPINB2 and AKR1C1, among the upregulated genes, as target for miR-182 and miR-185, respectively. Ectopic expression of each of these genes significantly enhanced foci formation in NIH3T3 cells. Following subcutaneous injection of these cells into nude mice, fibrosarcoma were formed from SLC30A1- or SERPINB2-expressing cells. Reduced plasma levels of miR-182 were detected in subjects exposed to high level of PM2.5 than in those exposed to low level of PM2.5 (P = 0.043). Similar results were seen for miR-185 although the difference was not statistically significant (P = 0.328). Increased expressions of SLC30A1, SERPINB2 and AKR1C1 were detected in human lung cancer. These results suggest that modulation of miR-182 and miR-185 and their target genes may contribute to lung carcinogenesis attributable to PM2.5 exposure.
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