ArticleJournal of experimental & clinical cancer research : CR2022
PM2.5 promotes NSCLC carcinogenesis through translationally and transcriptionally activating DLAT-mediated glycolysis reprograming.
Article in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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The trial behind it
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Who cites it
68 citing papers in PubMed, 121 citations in OpenAlex.
- tRNA-derived fragment AS-tDR-008272 promotes NSCLC tumorigenesis by propelling glycolytic metabolism via regulating HJURP.Translational oncology · 2026Article
- Hallmarks of lung cancer driven by inhalable particulate matter: From cell-intrinsic oncogenic traits to microenvironment remodeling.Innovation (Cambridge (Mass.)) · 2026Review
- Emerging role of copper in the pathophysiology of spinal cord injury.Neural regeneration research · 2026Article
- PMEnvironment & health (Washington, D.C.) · 2026Article
- Particulate matter 2.5 induced inflammatory responses and metabolic alterations in human monocytes.Scientific reports · 2026Article
- GSH-Responsive Nanoparticles Enhance Hepatocellular Carcinoma Immunotherapy Through Synergistic Effects of Cuproptosis and PI3K Inhibitor Combination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- AI-guided multi-omics analysis identifies NPC1-modulated susceptibility to SARS-CoV-2 infection under PMNature communications · 2026Article
- Review
- A comprehensive examination of the impact of environmental pollution on lung cancer: A review.Journal of advanced research · 2026Review
- Time-varying exposure to ambient air pollution and mortality among colon cancer patients in northern Thailand: a 15-year retrospective cohort study.Frontiers in public health · 2026Article
- Post-translational protein lactylation modification in lung cancer: an emerging targeted therapeutic strategy.Frontiers in immunology · 2026Review
- The inhibitory effect of hepatic cancer energy metabolism on immune checkpoint therapy: perspectives from single-cell multi-omics analysis.Frontiers in immunology · 2026Article
- Long-term exposure to PMThe Lancet. Planetary health · 2025Article
- Molecular signatures under hexavalent chromium, particulate matter 2.5, and cigarette smoking exposures.Discover oncology · 2025Article
- Gradual Increase in Lung Cancer Risk Due to Particulate Matter Exposure in Patients With Pulmonary Function Impairments: A Nationwide Korean Database Analysis.Journal of Korean medical science · 2025Article
- Protein lipoylation in cancer: metabolic reprogramming and therapeutic potential.Cell death discovery · 2025Review
- Article
- Particulate matter air pollution as a cause of lung cancer: epidemiological and experimental evidence.British journal of cancer · 2025Review
- The molecular mechanism and therapeutic landscape of copper and cuproptosis in cancer.Signal transduction and targeted therapy · 2025Review
- Endoplasmic reticulum stress related super-enhancers suppress cuproptosis via glycolysis reprogramming in lung adenocarcinoma.Cell death & disease · 2025Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAirborne fine particulate matter (PM2.5) has been associated with lung cancer development and progression in never smokers. However, the molecular mechanisms underlying PM2.5-induced lung cancer remain largely unknown. The aim of this study was to explore the mechanisms by which PM2.5 regulated the carcinogenesis of non-small cell lung cancer (NSCLC).
methodsParalleled ribosome sequencing (Ribo-seq) and RNA sequencing (RNA-seq) were performed to identify PM2.5-associated genes for further study. Quantitative real time-PCR (qRT-PCR), Western blot, and immunohistochemistry (IHC) were used to determine mRNA and protein expression levels in tissues and cells. The biological roles of PM2.5 and PM2.5-dysregulated gene were assessed by gain- and loss-of-function experiments, biochemical analyses, and Seahorse XF glycolysis stress assays. Human tissue microarray analysis and
resultsWe found that PM2.5 induced a translation shift towards glycolysis pathway genes and increased glycolysis metabolism, as evidenced by increased L-lactate and pyruvate concentrations or higher extracellular acidification rate (ECAR) in vitro and in vivo. Particularly, PM2.5 enhanced the expression of glycolytic gene DLAT, which promoted glycolysis but suppressed acetyl-CoA production and enhanced the malignancy of NSCLC cells. Clinically, high expression of DLAT was positively associated with tumor size, poorer prognosis, and SUVmax values of
conclusionsThis study demonstrated that PM2.5-activated overexpression of DLAT and enhancement in glycolysis metabolism contributed to the tumorigenesis of NSCLC, suggesting that DLAT-associated pathway may be a therapeutic target for NSCLC.
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