ReviewJournal of cancer prevention2025
The Role of Mesenchymal Stem Cells in Drug Resistance in Lung Neoplasms.
Review in Journal of cancer prevention, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Extracellular Vesicles in Diffuse Midline Glioma: Emerging Mediators of Radiation Response and Therapeutic Resistance.Cancers · 2026Review
- Rearming mesenchymal stem cells with engineering strategies to combat cancer.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor microenvironment (TME) is a decisive determinant of therapeutic response and the emergence of drug resistance in lung cancer. Among its stromal constituents, mesenchymal stem cells (MSCs) are pivotal regulators of disease progression because they secrete diverse paracrine mediators. Accumulating evidence indicates that MSC-derived cytokines, growth factors, and extracellular vesicles (EVs) drive epithelial-mesenchymal transition (EMT)-a phenotypic shift that augments cellular motility, invasiveness, and stem-like traits. EMT contributes directly to resistance against epidermal growth factor receptor tyrosine kinase inhibitors and platinum-based chemotherapy. Key MSC-secreted factors, such as TGF-β1, interleukin-6, and C-C motif chemokine ligand 5, activate signal transducer and activator of transcription 3, phosphoinositide 3-kinase/AKT, and Wnt/β-catenin cascades, thereby reinforcing drug-resistant phenotypes. MSC-induced EMT also remodels immune surveillance and supports the persistence of residual tumor clones. Elucidating the molecular reciprocity between MSCs and lung cancer cells within the TME is indispensable for rational therapy design. This review synthesizes current mechanistic insights into MSC-mediated EMT-driven resistance and discusses translational strategies including targeted inhibition of paracrine signaling and EV engineering that may restore drug sensitivity in lung cancer.
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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.