ArticleCancer biology & therapy2014
Enhanced shedding of extracellular vesicles from amoeboid prostate cancer cells: potential effects on the tumor microenvironment.
Article in Cancer biology & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Diagnostic, prognostic and predictive value of cell-free miRNAs in prostate cancer: a systematic review.Molecular cancer · 2016Pooled it
- Extracellular vesicles in prostate cancer: current understanding and future perspectives.Journal of the National Cancer Center · 2026Review
- Transforming Cancer Care with Oncosomes: Insight into Biogenesis, Functional Role, and Therapeutic Potential.Pharmaceutics · 2026Review
- DIAPH3 is a multifaceted prognostic biomarker that links immunotherapy response to tumor microenvironment in prostate cancer.Discover oncology · 2026Article
- Mechanical regulation of extracellular vesicle activity during tumour progression.Nature biomedical engineering · 2025Review
- Role of Redox Homeostasis in the Communication Between Brain and Liver Through Extracellular Vesicles.Antioxidants (Basel, Switzerland) · 2024Review
- Applications of Urinary Extracellular Vesicles in the Diagnosis and Active Surveillance of Prostate Cancer.Cancers · 2024Review
- Role of actin-binding proteins in prostate cancer.Frontiers in cell and developmental biology · 2024Review
- Clinical significance of small extracellular vesicles in cholangiocarcinoma.Frontiers in oncology · 2024Review
- Enhancement of dielectrophoresis-based particle collection from high conducting fluids due to partial electrode insulation.Electrophoresis · 2023Article
- Folylpolyglutamate synthetase mRNA G-quadruplexes regulate its cell protrusion localization and enhance a cancer cell invasive phenotype upon folate repletion.BMC biology · 2023Article
- DIAPH3 is a prognostic biomarker and inhibit colorectal cancer progression through maintaining EGFR degradation.Cancer medicine · 2022Article
- Extracellular signals regulate the biogenesis of extracellular vesicles.Biological research · 2022Review
- CircRNA/miRNA/mRNA axis participates in the progression of partial bladder outlet obstruction.BMC urology · 2022Article
- Exosomal MicroRNAs as Novel Cell-Free Therapeutics in Tissue Engineering and Regenerative Medicine.Biomedicines · 2022Review
- Molecular mechanisms and clinical applications of exosomes in prostate cancer.Biomarker research · 2022Review
- Microparticles: biogenesis, characteristics and intervention therapy for cancers in preclinical and clinical research.Journal of nanobiotechnology · 2022Review
- Role of extracellular vesicles in osteosarcoma.International journal of medical sciences · 2022Review
- Article
- Communication between cells: exosomes as a delivery system in prostate cancer.Cell communication and signaling : CCS · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
The gene encoding the cytoskeletal regulator DIAPH3 is lost at high frequency in metastatic prostate cancer, and DIAPH3 silencing evokes a transition to an amoeboid tumor phenotype in multiple cell backgrounds. This amoeboid transformation is accompanied by increased tumor cell migration, invasion, and metastasis. DIAPH3 silencing also promotes the formation of atypically large (> 1 μm) membrane blebs that can be shed as extracellular vesicles (EV) containing bioactive cargo. Whether loss of DIAPH3 also stimulates the release of nano-sized EV (e.g., exosomes) is not established. Here we examined the mechanism of release and potential biological functions of EV shed from DIAPH3-silenced and other prostate cancer cells. We observed that stimulation of LNCaP cells with the prostate stroma-derived growth factor heparin-binding EGF-like growth factor (HB-EGF), combined with p38MAPK inhibition caused EV shedding, a process mediated by ERK1/2 hyperactivation. DIAPH3 silencing in DU145 cells also increased rates of EV production. EV isolated from DIAPH3-silenced cells activated AKT1 and androgen signaling, increased proliferation of recipient tumor cells, and suppressed proliferation of human macrophages and peripheral blood mononuclear cells. DU145 EV contained miR-125a, which suppressed AKT1 expression and proliferation in recipient human peripheral blood mononuclear cells and macrophages. Our findings suggest that EV produced as a result of DIAPH3 loss or growth factor stimulation may condition the tumor microenvironment through multiple mechanisms, including the proliferation of cancer cells and suppression of tumor-infiltrating immune cells.
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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 OpenQuestion graph.