ArticleBMC cancer2025
TRPM2 channels mediate ROS-induced actin remodeling and cell migration of prostate cancer cells.
Article in BMC cancer, 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
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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.
- Pathophysiological significance of the TRPM2 ion channel as a potential target in cancer, neurological disorders, and ischemia/reperfusion injury.Pharmacological research · 2026Review
- Reactive Oxygen Species Drive Cell Migration and PD-L1 Expression via YB-1 Phosphorylation in Pleural Mesothelioma.Antioxidants (Basel, Switzerland) · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundActin remodeling plays important roles in pathophysiological processes such as cancer metastasis and angiogenesis. Reactive oxygen species (ROS) are signaling molecules thought to regulate cell migration by remodeling actin cytoskeleton. Earlier, we demonstrated that Transient receptor potential melastatin 2 (TRPM2) channels mediates H
methodsThe study utilized various molecular probes, reagents, and cell culture techniques. Prostate cancer (PC)-3 and DU145 cell line were cultured and treated with different compounds to induce ROS production and actin remodeling. The actin cytoskeleton was stained with phalloidin or labelled with pActin-tdTomato plasmid and imaged using confocal microscopy. Zn
resultsWe demonstrated that both H
conclusionsTRPM2 channels and TRPM2-mediated Zn
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Registered trials
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