ArticleiScience2025
Mesenchymal-epithelial transition reduces proliferation but increases immune evasion in tumor spheroids.
Article in iScience, 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
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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.
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Who cites it
2 citing papers in PubMed.
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- Targeting Matrix Stiffness and Mechanotransduction in Breast Cancer: Implications for Emerging Therapies.International journal of molecular sciences · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mesenchymal-epithelial transition (MET) whether full or partial, has been implicated in secondary tumor growth during metastasis. Here, we explore whether MET enhances tumor outgrowth by boosting proliferation, using MET-inducible mesenchymal cancer cell lines. Surprisingly, we found that crowding inhibition of proliferation persists both before and after MET, however, escaping crowding conferred a proliferative advantage to mesenchymal cells. In three-dimensional culture, MET caused a reduction in proliferation, accompanied by changes in proliferative signaling of focal adhesions and actomyosin. Furthermore, co-culture experiments with peripheral blood mononuclear cells revealed that MET-induced spheroids demonstrate an increased evasion to immune cell attack. This effect is likely mediated by both a confined morphology and alterations in the expression of key immunomodulatory molecules. Together, these findings suggest that MET may contribute to secondary tumor outgrowth, not by boosting proliferation, but by enhancing survival in immune-challenging environments.
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Registered trials
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