Evidence map›Paper›PMID 33473262›Full record

ArticleJournal of extracellular vesicles2021

Cdc42 functions as a regulatory node for tumour-derived microvesicle biogenesis.

Jing Wang, Xiangjin Zhuang, Kai Su Greene, Ha Si, Marc A Antonyak, Joseph E Druso, Kristin F Wilson, Richard A Cerione, Qiyu Feng, Hongyang Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of extracellular vesicles, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  4. The pathophysiological role of MiRNAs in heart failure.Frontiers in cardiovascular medicine · 2026
    Review
  5. Review
  6. Article
  7. Review
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  12. Role of scaffold proteins in the heterogeneity of glioblastoma.Cell communication and signaling : CCS · 2024
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Breaking free: endocytosis and endosomal escape of extracellular vesicles.Extracellular vesicles and circulating nucleic acids · 2023
    Review
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

10 authors at 4 institutions in 2 countries.

Jing WangCancer Research Center The First Affiliated Hospital of USTC Division of Life Sciences and Medicine University of Science and Technology of China Hefei Anhui China.
Xiangjin ZhuangCancer Research Center The First Affiliated Hospital of USTC Division of Life Sciences and Medicine University of Science and Technology of China Hefei Anhui China.
Kai Su GreeneDepartment of Molecular Medicine Cornell University Ithaca New York USA.
Ha SiNational Center for Liver Cancer Eastern Hepatobiliary Surgery Hospital/Institute the Second Military Medical University Shanghai China.
Marc A AntonyakDepartment of Molecular Medicine Cornell University Ithaca New York USA.
Joseph E DrusoDepartment of Molecular Medicine Cornell University Ithaca New York USA.
Kristin F WilsonDepartment of Molecular Medicine Cornell University Ithaca New York USA.
Richard A CerioneDepartment of Molecular Medicine Cornell University Ithaca New York USA.
Qiyu FengCancer Research Center The First Affiliated Hospital of USTC Division of Life Sciences and Medicine University of Science and Technology of China Hefei Anhui China.
Hongyang WangCancer Research Center The First Affiliated Hospital of USTC Division of Life Sciences and Medicine University of Science and Technology of China Hefei Anhui China.
Cornell University · USEastern Hepatobiliary Surgery Hospital · CNUniversity of Science and Technology of China · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumour-derived microvesicles (MVs) serve as critical mediators of cell-to-cell communication in the tumour microenvironment. So far, the underlying mechanisms of MV biogenesis, especially how key tumorigenesis signals such as abnormal EGF signalling regulates MV release, remain unclear. Here, we set out to establish reliable readouts for MV biogenesis and then explore the molecular mechanisms that regulate MV generation. We found that Rho family small G protein Cdc42 is a convergent node of multiple regulatory signals that occur in MV biogenesis. The binding of activated GTP-bound Cdc42 and its downstream effector, Ras GTPase-activating-like protein 1 (IQGAP1), is required for MV shedding. Activated Cdc42 maintains sustained EGF signalling by inhibiting the internalization of cell surface receptors, including EGFR and the VEGF oligomer, VEGF

Indexed as

Tumor Microenvironment3T3 CellsAnimalscdc42 GTP-Binding ProteinCell CommunicationCell-Derived MicroparticlesCell LineCell Line, TumorExtracellular VesiclesHumansMiceNeoplasmsNeovascularization, Pathologicras GTPase-Activating ProteinsSignal Transductioncdc42 GTP-Binding ProteinCDC42 protein, humanras GTPase-Activating ProteinsCdc42EGF signallingGTPaseIQGAPMicrovesicletumour angiogenesis

Identifiers

PMID33473262
PMCPMC7804048
OpenAlexW3119362551

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.