ArticleScientific reports2025
The inhibitory effect of M2 macrophage-derived exosomes on gefitinib resistant lung adenocarcinoma cells through the MIF/TIMP1/CD74 axis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed.
- Integration of multi-omics and machine learning to identify core genes in PANoptosisof lung adenocarcinoma and their mechanisms in the tumor microenvironment and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Bridging Inflammation and Oncology: The Role and Therapeutic Potential of Macrophage Migration Inhibitory Factor in Lung Cancer.International journal of molecular sciences · 2026Review
- Overexpression of ANAPC1 Affects the Cell Cycle Pathway to Promote the Progression of Lung Adenocarcinoma.Combinatorial chemistry & high throughput screening · 2026Article
- Review
- Tumor-Associated Macrophages in Lung Cancer: Origins, Functional Heterogeneity, and Therapeutic Implications.Journal of inflammation research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung adenocarcinoma (LA) ranks among the most common malignant tumors worldwide. M2 macrophage-derived exosomes have been implicated in regulating LA progression and drug resistance. However, whether proteins encapsulated in these exosomes contribute to gefitinib resistance in LA remains to be elucidated. This study investigates the role of tissue inhibitor of metalloproteinase 1 (TIMP1) in mediating LA resistance to gefitinib. We demonstrated that M2 macrophages-derived exosomes enhanced the sensitivity of gefitinib-resistant LA cell lines (P < 0.05). Bioinformatics analyses validated the correlation of TIMP1 expression with LA progression and patient survival. Depletion of TIMP1 in M2 macrophage-derived exosomes suppressed the proliferation of gefitinib-resistant LA cells. Additionally, we confirmed that TIMP1 interacts with cluster of differentiation 74 (CD74), a process linked to the proliferation and migration of gefitinib-resistant LA cells. Additionally, this study validated that TIMP1 mediates the interaction between CD74 and macrophage migration inhibitory factor (MIF), potentially activating the PI3K/AKT signaling pathway. Collectively, these findings demonstrate that TIMP1 in M2 macrophage-derived exosomes facilitate the binding of MIF to CD74 in LA cells, thereby attenuating gefitinib resistance.
Indexed as
Identifiers
What OpenQuestion holds
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.