Evidence map›Paper›PMID 40571315›Full record

ArticleCancer genomics & proteomics2025

Particulate Matter 2.5 Induces FGFR1-mediated Integrin Switch to Promote Non-small Cell Lung Cancer Metastasis.

Nithikoon Aksorn, Zin Zin Ei, Korrakod Petsri, Narumon Phaonakrop, Chalermpong Saenjum, Sittiruk Roytrakul, Pithi Chanvorachote

Abstract read
In one paragraph

Article in Cancer genomics & proteomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Nithikoon AksornDepartment of Clinical Pathology, Faculty of Medicine Vajira Hospital, Navamindradhiraj University, Bangkok, Thailand.
Zin Zin EiDepartment of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand.
Korrakod PetsriDepartment of Pharmacology, Faculty of Medicine, Kasetsart University, Bangkok, Thailand.
Narumon PhaonakropFunctional Proteomics Technology Laboratory, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathum Thani, Thailand.
Chalermpong SaenjumDepartment of Pharmaceutical Sciences, Faculty of Pharmacy, Chiang Mai University, Chiang Mai, Thailand.
Sittiruk RoytrakulFunctional Proteomics Technology Laboratory, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathum Thani, Thailand.
Pithi ChanvorachoteDepartment of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand; pithi.c@chula.ac.th pithi_chan@yahoo.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimParticulate matter 2.5 (PM2.5) is known to adversely affect human health. While its involvement in lung cancer pathogenesis is recognized, its specific impact on metastasis-related behaviors of lung cancer cells remains largely unexplored. MATERIALS AND

methodsIn this study, we employed cell culture models, proteomic analysis, and bioinformatic analysis. Target proteins and signaling pathways were validated using western blotting and immunofluorescence assay. Wound healing, transwell migration and phalloidin-rhodamine assays were used to determine the migratory activity.

resultsProteomic analysis identified 3,795 proteins in both control and PM2.5-treated groups. Among these, proteins associated with metastasis, particularly those related to "cell migration" (GO: 0016477), were highlighted, identifying six key proteins involved in cancer metastasis. Protein-protein interaction analysis pinpointed fibroblast growth factor receptor 1 (FGFR1) as a central target influenced by PM2.5, which promoted cell migration

conclusionThese results indicate that FGFR1 is a crucial target in PM2.5-induced metastasis in lung cancer cells, operating through an FGFR1/integrin/Akt signaling axis. This study advances our understanding of the role of PM2.5 in lung cancer metastasis and suggests potential therapeutic strategies to mitigate cancer progression.

Indexed as

Carcinoma, Non-Small-Cell LungIntegrinsLung NeoplasmsParticulate MatterReceptor, Fibroblast Growth Factor, Type 1Cell Line, TumorCell MovementHumansNeoplasm MetastasisProteomicsSignal TransductionFGFR1 protein, humanIntegrinsParticulate MatterReceptor, Fibroblast Growth Factor, Type 1FGFR1lung cancermetastasisParticulate matter 2.5PM2.5proteomics

Identifiers

PMID40571315
PMCPMC12216578

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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.