Evidence map›Paper›PMID 24310399›Full record

ArticleCancer research2014

Extracellular vesicles modulate the glioblastoma microenvironment via a tumor suppression signaling network directed by miR-1.

Agnieszka Bronisz, Yan Wang, Michal O Nowicki, Pierpaolo Peruzzi, Khairul Ansari, Daisuke Ogawa, Leonora Balaj, Gianluca De Rienzo, Marco Mineo, Ichiro Nakano and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed
8.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

148 citing papers in PubMed, 228 citations in OpenAlex.

  1. Review
  2. Extracellular vesicles: Navigating new frontiers in glioblastoma therapy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Glioma-Derived Exosomes and Their Application as Drug Nanoparticles.International journal of molecular sciences · 2024
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Exosomes as Novel Diagnostic Biomarkers and Therapeutic Tools in Gliomas.International journal of molecular sciences · 2023
    Review
  19. Review
  20. Review

88 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 1 country.

Agnieszka Bronisz *Harvey Cushing Neuro-oncology Laboratories, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Yan Wang *Department of Neurological Surgery, the Ohio State University Medical Center, Columbus, OH 43210, USA.
Michal O NowickiHarvey Cushing Neuro-oncology Laboratories, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Pierpaolo PeruzziDepartment of Neurological Surgery, the Ohio State University Medical Center, Columbus, OH 43210, USA.
Khairul AnsariHarvey Cushing Neuro-oncology Laboratories, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Daisuke OgawaHarvey Cushing Neuro-oncology Laboratories, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Leonora BalajNeuroscience Center at Massachusetts General Hospital, Charlestown, MA 02129.
Gianluca De RienzoHarvey Cushing Neuro-oncology Laboratories, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Marco MineoHarvey Cushing Neuro-oncology Laboratories, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Ichiro NakanoDepartment of Neurological Surgery, the Ohio State University Medical Center, Columbus, OH 43210, USA.
Michael C OstrowskiDepartment of Molecular and Cellular Biochemistry, the Ohio State University Medical Center, Columbus, OH 43210, USA.
Fred HochbergNeuroscience Center at Massachusetts General Hospital, Charlestown, MA 02129.
Ralph WeisslederNeuroscience Center at Massachusetts General Hospital, Charlestown, MA 02129.
Sean E LawlerHarvey Cushing Neuro-oncology Laboratories, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
E Antonio ChioccaHarvey Cushing Neuro-oncology Laboratories, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Jakub GodlewskiHarvey Cushing Neuro-oncology Laboratories, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Harvard University · USThe Ohio State University Wexner Medical Center · USMassachusetts General Hospital · USNeurological Surgery · USThe Ohio State University · USBrigham and Women's Hospital · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Daniel G. Stover · 1985 to 2026
$132.3M
The role of microvesicles in giloma virotherapyP01CA069246 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI CHIOCCA, E. ANTONIO · 1996 to 2021
$30.9M
The Tumor Microenvironmental Barrier to Effective Viral OncolysisP01CA163205 · NCI · OHIO STATE UNIVERSITY · PI Xiaokui Mo · 2013 to 2026
$26.0M
Suppression of Mammary Tumorigenesis by Stromal p53P01CA097189 · NCI · OHIO STATE UNIVERSITY · PI ROSOL, THOMAS J · 2004 to 2016
$16.1M
NCI NIH HHS P01 CA069246NCI NIH HHS P01 CA097189NCI NIH HHS P01 CA163205NCI NIH HHS P30 CA016058
6 · The paper itself

Abstract

Extracellular vesicles have emerged as important mediators of intercellular communication in cancer, including by conveying tumor-promoting microRNAs between cells, but their regulation is poorly understood. In this study, we report the findings of a comparative microRNA profiling and functional analysis in human glioblastoma that identifies miR-1 as an orchestrator of extracellular vesicle function and glioblastoma growth and invasion. Ectopic expression of miR-1 in glioblastoma cells blocked in vivo growth, neovascularization, and invasiveness. These effects were associated with a role for miR-1 in intercellular communication in the microenvironment mediated by extracellular vesicles released by cancer stem-like glioblastoma cells. An extracellular vesicle-dependent phenotype defined by glioblastoma invasion, neurosphere growth, and endothelial tube formation was mitigated by loading miR-1 into glioblastoma-derived extracellular vesicles. Protein cargo in extracellular vesicles was characterized to learn how miR-1 directed extracellular vesicle function. The mRNA encoding Annexin A2 (ANXA2), one of the most abundant proteins in glioblastoma-derived extracellular vesicles, was found to be a direct target of miR-1 control. In addition, extracellular vesicle-derived miR-1 along with other ANXA2 extracellular vesicle networking partners targeted multiple pro-oncogenic signals in cells within the glioblastoma microenvironment. Together, our results showed how extracellular vesicle signaling promotes the malignant character of glioblastoma and how ectopic expression of miR-1 can mitigate this character, with possible implications for how to develop a unique miRNA-based therapy for glioblastoma management.

Indexed as

AnimalsBiological TransportBrain NeoplasmsCell Line, TumorCell MovementDisease Models, AnimalExosomesFemaleGene ExpressionGene Expression Regulation, NeoplasticGlioblastomaHumansMiceMicroRNAsNeoplasm InvasivenessNeovascularization, PathologicMicroRNAsMIRN1 microRNA, human

Identifiers

PMID24310399
PMCPMC3928601
OpenAlexW1978118502

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.