ArticleScientific reports2024
Nuclear rupture induced by capillary constriction forces promotes differential effects on metastatic and normal breast cells.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- Nuclear envelope rupture and resealing: mechanisms, consequences, and disease implications.Biochemical Society transactions · 2026Review
- Actin cytoskeleton protection by the formin-mediated safety valve.Current opinion in cell biology · 2025Review
- Capillary constrictions prime cancer cell tumorigenicity through PIEZO1.Nature communications · 2025Article
- The Mechanical Properties of Breast Cancer Cells and Their Surrounding Microenvironment.International journal of molecular sciences · 2025Review
- The Secretome of the Inductive Tooth Germ Exhibits Signals Required for Tooth Development.Bioengineering (Basel, Switzerland) · 2025Article
- Clinicopathologic Characteristics of Intraglomerular Malignancy in Kidney Biopsies.Glomerular diseasesArticle
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
During metastatic dissemination, circulating tumour cells (CTCs) enter capillary beds, where they experience mechanical constriction forces. The transient and persistent effects of these forces on CTCs behaviour remain poorly understood. Here, we developed a high-throughput microfluidic platform mimicking human capillaries to investigate the impact of mechanical constriction forces on malignant and normal breast cell lines. We observed that capillary constrictions induced nuclear envelope rupture in both cancer and normal cells, leading to transient changes in nuclear and cytoplasmic area. Constriction forces transiently activated cGAS/STING and pathways involved in inflammation (NF-κB, STAT and IRF3), especially in the non-malignant cell line. Furthermore, the non-malignant cell line experienced transcriptional changes, particularly downregulation of epithelial markers, while the metastatic cell lines showed minimal alterations. These findings suggest that mechanical constriction forces within capillaries may promote differential effects in malignant and normal cell lines.
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Registered trials
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