ArticlePloS one2015
Galectin-3 Overrides PTRF/Cavin-1 Reduction of PC3 Prostate Cancer Cell Migration.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 38 citations in OpenAlex.
- Orchestrating movement: the role of Caveolin-1 in migration and metastasis.Molecular cancer · 2025Review
- Scaffolds and the scaffolding domain: an alternative paradigm for caveolin-1 signaling.Biochemical Society transactions · 2024Review
- The Cavin-1/Caveolin-1 interaction attenuates BMP/Smad signaling in pulmonary hypertension by interfering with BMPR2/Caveolin-1 binding.Communications biology · 2024Article
- The critical roles of caveolin-1 in lung diseases.Frontiers in pharmacology · 2024Review
- Caveolar and non-Caveolar Caveolin-1 in ocular homeostasis and disease.Progress in retinal and eye research · 2022Review
- Overcoming Microenvironment-Mediated Chemoprotection through Stromal Galectin-3 Inhibition in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2021Article
- Single molecule network analysis identifies structural changes to caveolae and scaffolds due to mutation of the caveolin-1 scaffolding domain.Scientific reports · 2021Article
- Integrated Bioinformatic Analysis of the Expression and Prognosis of Caveolae-Related Genes in Human Breast Cancer.Frontiers in oncology · 2021Article
- Lessons from cavin-1 deficiency.Biochemical Society transactions · 2020Review
- Homotrimer cavin1 interacts with caveolin1 to facilitate tumor growth and activate microglia through extracellular vesicles in glioma.Theranostics · 2020Article
- Galectins in prostate and bladder cancer: tumorigenic roles and clinical opportunities.Nature reviews. Urology · 2019Review
- Correlation of the invasive potential of glioblastoma and expression of caveola-forming proteins caveolin-1 and CAVIN1.Journal of neuro-oncology · 2019Article
- Caveolae and scaffold detection from single molecule localization microscopy data using deep learning.PloS one · 2019Article
- The role of PTRF/Cavin1 as a biomarker in both glioma and serum exosomes.Theranostics · 2018Article
- The phospho-caveolin-1 scaffolding domain dampens force fluctuations in focal adhesions and promotes cancer cell migration.Molecular biology of the cell · 2017Article
- Abituzumab Targeting of αV-Class Integrins Inhibits Prostate Cancer Progression.Molecular cancer research : MCR · 2017Article
- Prostate tumor DNA methylation is associated with cigarette smoking and adverse prostate cancer outcomes.Cancer · 2016Article
- Galectin-3 Determines Tumor Cell Adaptive Strategies in Stressed Tumor Microenvironments.Frontiers in oncology · 2016Review
- Myocardin Family Members Drive Formation of Caveolae.PloS one · 2015Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Expression of Caveolin-1 (Cav1), a key component of cell surface caveolae, is elevated in prostate cancer (PCa) and associated with PCa metastasis and a poor prognosis for PCa patients. Polymerase I and Transcript Release Factor (PTRF)/cavin-1 is a cytoplasmic protein required for Cav1-dependent formation of caveolae. Expression of PTRF reduces the motility of PC3 cells, a metastatic prostate cancer cell line that endogenously expresses abundant Cav1 but no PTRF and no caveolae, suggesting a role for non-caveolar Cav1 domains, or Cav1 scaffolds, in PCa cell migration. Tyrosine phosphorylated Cav1 (pCav1) functions in concert with Galectin-3 (Gal3) and the galectin lattice to stabilize focal adhesion kinase (FAK) within focal adhesions (FAs) and promote cancer cell motility. However, whether PTRF regulation of Cav1 function in PCa cell migration is related to Gal3 expression and functionality has yet to be determined. Here we show that PTRF expression in PC3 cells reduces FAK stabilization in focal adhesions and reduces cell motility without affecting pCav1 levels. Exogenous Gal3 stabilized FAK in focal adhesions of PTRF-expressing cells and restored cell motility of PTRF-expressing PC3 cells to levels of PC3 cells in a dose-dependent manner, with an optimal concentration of 2 µg/ml. Exogenous Gal3 stabilized FAK in focal adhesions of Gal3 knockdown PC3 cells but not in Cav1 knockdown PC3 cells. Cav1 knockdown also prevented Gal3 rescue of FA-associated FAK stabilization in PTRF-expressing PC3 cells. Our data support a role for PTRF/cavin-1, through caveolae formation, as an attenuator of the non-caveolar functionality of Cav1 in Gal3-Cav1 signalling and regulation of focal adhesion dynamics and cancer cell migration.
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