ArticleOncotarget2016
Repeated PM2.5 exposure inhibits BEAS-2B cell P53 expression through ROS-Akt-DNMT3B pathway-mediated promoter hypermethylation.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 116 citations in OpenAlex.
- Airborne Particulate Matter as an Emerging Driver of Gastric Carcinogenesis: Molecular Pathways Linking Inflammation and Cancer.International journal of molecular sciences · 2026Review
- Differential toxicity of water- and DMSO-extractable PM2.5 fractions in human alveolar organoids.Frontiers in toxicology · 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
- Prenatal Exposure to Fine Particulate Matter Components and Autism Risk in Childhood.JAMA network open · 2025Article
- Rewriting nuclear epigenetic scripts in mitochondrial diseases as a strategy for heteroplasmy control.EMBO molecular medicine · 2025Article
- Environmental interpretation of the impact of vehicle emissions on prostate cancer progression.Cancer cell international · 2025Article
- Particulate matter air pollution as a cause of lung cancer: epidemiological and experimental evidence.British journal of cancer · 2025Review
- Differential regulation of calcium-NFAT signaling pathway by Akt isoforms: unraveling effector dynamics and exhaustion of cytotoxic T lymphocytes in tumor microenvironment.Journal for immunotherapy of cancer · 2025Article
- Unraveling the mechanisms underlying air pollution-induced dysfunction of the oral-gut-brain axis: implications for human health and well-being.Asian biomedicine : research, reviews and news · 2025Review
- Lung cancer associated with combustion particles and fine particulate matter (PMBiochemical pharmacology · 2023Review
- Additive effects of 10-year exposures to PMEnvironmental epidemiology (Philadelphia, Pa.) · 2023Article
- Korean Red Ginseng Attenuates Particulate Matter-Induced Senescence of Skin Keratinocytes.Antioxidants (Basel, Switzerland) · 2023Article
- The impact of social and environmental factors on cancer biology in Black Americans.Cancer causes & control : CCC · 2023Review
- The Road to Malignant Cell Transformation after Particulate Matter Exposure: From Oxidative Stress to Genotoxicity.International journal of molecular sciences · 2023Review
- Epigenetic mechanisms of particulate matter exposure: air pollution and hazards on human health.Frontiers in genetics · 2023Review
- The Role of Neighborhood Air Pollution Exposure on Somatic Non-Small Cell Lung Cancer Mutations in the Los Angeles Basin (2013-2018).International journal of environmental research and public health · 2022Article
- Emerging Insights into the Impact of Air Pollution on Immune-Mediated Asthma Pathogenesis.Current allergy and asthma reports · 2022Review
- Real-world PMEnvironmental science and pollution research international · 2022Article
- Respiratory exposure to PM2.5 soluble extract induced chronic lung injury by disturbing the phagocytosis function of macrophage.Environmental science and pollution research international · 2022Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term exposure to fine particulate matter (PM2.5) has been reported to be closely associated with the increased lung cancer risk in populations, but the mechanisms underlying PM-associated carcinogenesis are not yet clear. Previous studies have indicated that aberrant epigenetic alterations, such as genome-wide DNA hypomethylation and gene-specific DNA hypermethylation contribute to lung carcinogenesis. And silence or mutation of P53 tumor suppressor gene is the most prevalent oncogenic driver in lung cancer development. To explore the effects of PM2.5 on global and P53 promoter methylation changes and the mechanisms involved, we exposed human bronchial epithelial cells (BEAS-2B) to low concentrations of PM2.5 for 10 days. Our results indicated that PM2.5-induced global DNA hypomethylation was accompanied by reduced DNMT1 expression. PM2.5 also induced hypermethylation of P53 promoter and inhibited its expression by increasing DNMT3B protein level. Furthermore, ROS-induced activation of Akt was involved in PM2.5-induced increase in DNMT3B. In conclusion, our results strongly suggest that repeated exposure to PM2.5 induces epigenetic silencing of P53 through ROS-Akt-DNMT3B pathway-mediated promoter hypermethylation, which not only provides a possible explanation for PM-induced lung cancer, but also may help to identify specific interventions to prevent PM-induced lung carcinogenesis.
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