ArticleScientific reports2025
Focal adhesion assembly and cell migration require myoferlin in PDAC cell lines.
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 3 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Review
- Myoferlin at the crossroad of vesicle trafficking and mitochondrial function: implications for pancreatic cancer progression and stromal reprogramming.Biochemical Society transactions · 2026Review
- Myoferlin contributes to invasiveness of human T-cell leukemia virus type 1-infected T cells.Journal of virology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) has a dire prognosis due to late diagnosis and ineffective treatments. Myoferlin, a transmembrane protein, is overexpressed in PDAC and correlates with poor patient survival, making it a potential therapeutic target. Several reports indicated that myoferlin depletion in cancer cells reduced migration or metastatic dissemination, but they failed to provide a consistent mechanism. Understanding the biology behind the dissemination of PDAC is of outmost importance, as this disease is often diagnosed at an advanced stage. This study aims to further elucidate myoferlin's role in cell migration. Myoferlin expression in PDAC patients correlated with gene sets related to the actin cytoskeleton, and myoferlin knockdown in PDAC cell lines similarly affected these gene sets. Electron microscopy revealed that myoferlin depletion altered cytoskeleton ultrastructure. Immunofluorescence confirmed that myoferlin knockdown disorganized microfilaments, despite not altering β-actin abundance. Functionally, myoferlin depletion significantly reduced PDAC cell migration. While core machinery for actin polymerization/depolymerization and EMT markers remained unaffected, myoferlin knockdown increased the abundance of focal adhesion components. However, immunofluorescence showed a decrease in the number of functional focal adhesions, with paxillin accumulating in the cytosol. Cell migration relies on the dynamics of focal adhesions. The reduction in functional focal adhesions indicates that the cell has fewer points of attachment for migration. We suggest this impairment was linked to a significant decrease in clathrin heavy chain abundance and pointed to a disrupted clathrin-mediated endocytosis. This study highlights a novel role for myoferlin in focal adhesion recycling in PDAC and provides a consistent mechanism explaining how myoferlin contributes to PDAC cell migration, a significant event in metastatic dissemination, and reinforce its potential as a therapeutic target.
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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 Socratic graph.