ArticleInternational journal of biological sciences2024
Particulate matter facilitates amphiregulin-dependent lung cancer proliferation through glutamine metabolism.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed.
- Hallmarks of lung cancer driven by inhalable particulate matter: From cell-intrinsic oncogenic traits to microenvironment remodeling.Innovation (Cambridge (Mass.)) · 2026Review
- Cancer and aging: complex associations and therapeutic targets.Molecular biomedicine · 2026Review
- Betulin inhibits inflammatory factors synthesis in osteoarthritis synovial fibroblasts by suppressing the PI3K, Akt, and mTOR pathways and activating miR-5006-5p.International journal of medical sciences · 2026Article
- Long Noncoding RNA Lnc-MTPAP-1 Overexpressed by Particulate Matter Suppresses Apoptosis in Non-Small Cell Lung Cancer (NSCLC) Cells.International journal of molecular sciences · 2025Article
- Article
- Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025Review
- Targeting glutamine metabolism as a potential target for cancer treatment.Journal of experimental & clinical cancer research : CR · 2025Review
- Cell Death and Proliferation Variability Caused by Different Dust Clay Minerals Using the Single-Cell Method.GeoHealth · 2025Article
- Joint exposure to PMFrontiers in public health · 2025Article
- Hyodeoxycholic acid inhibits colorectal cancer proliferation through the FXR/EREG/EGFR axis.Frontiers in cell and developmental biology · 2024Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although many cohort studies have reported that long-term exposure to particulate matter (PM) causes lung cancer, the molecular mechanisms underlying the PM-induced increases in lung cancer progression remain unclear. We applied the lung cancer cell line A549 (Parental; A549.Par) to PM for an extended period to establish a mimic PM-exposed lung cancer cell line, A549.PM. Our results indicate that A549.PM exhibits higher cell growth and proliferation abilities compared to A549.Par cells
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.