Evidence map›Paper›PMID 30279961›Full record

ArticleOncotarget2018

The vesicular transfer of CLIC1 from glioblastoma to microvascular endothelial cells requires TRPM7.

Dominique Thuringer, Gaetan Chanteloup, Pascale Winckler, Carmen Garrido

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Roles of TRPM channels in glioma.Cancer biology & therapy · 2024
    Review
  3. The Role of TRPM7 in Oncogenesis.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
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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

4 authors at 3 institutions in 1 country.

Dominique ThuringerINSERM U1231, Laboratory of Excellence Ligue Nationale contre le Cancer, 21000 Dijon, France.
Gaetan ChanteloupINSERM U1231, Laboratory of Excellence Ligue Nationale contre le Cancer, 21000 Dijon, France.
Pascale WincklerAgroSup Dijon, PAM UMR, DImaCell Imaging Facility, Université de Bourgogne Franche Comté, 21000 Dijon, France.
Carmen GarridoINSERM U1231, Laboratory of Excellence Ligue Nationale contre le Cancer, 21000 Dijon, France.
La Ligue Contre le Cancer · FRInstitut Agro Dijon · FRUniversité Bourgogne Franche-Comté · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chloride intracellular channel 1 (CLIC1) is highly expressed and secreted by human glioblastoma cells and cell lines such as U87, initiating cell migration and tumor growth. Here, we examined whether CLIC1 could be transferred to human primary microvascular endothelial cells (HMEC). We previously reported that the oncogenic microRNA, miR-5096, increased the release of extracellular vesicles (EVs) by which it increased its own transfer from U87 to surrounding cells. Thus, we also examined its effect on the CLIC1 transfer. In homotypic cultures, miR-5096 did not increase the expression of CLIC1 in U87 nor in HMEC. However, the endothelial CLIC1 level increased after exposure to EVs released by U87, and even more by miR-5096-loaded U87. The EVs-transferred CLIC1 was active in HMEC, promoting endothelial sprouting in matrigel. Cell exposure to EVs induced cytosolic Ca

Indexed as

chloride intracellular channelexosomeglioblastomamicroRNAtransient receptor potential melastatin

Identifiers

PMID30279961
PMCPMC6161795
OpenAlexW2892360547

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.