Evidence map›Paper›PMID 36647117›Full record

ArticleActa neuropathologica communications2023

CIC reduces xCT/SLC7A11 expression and glutamate release in glioma.

Jong-Whi Park, Omer Kilic, Minh Deo, Kevin Jimenez-Cowell, Engin Demirdizen, Hyunggee Kim, Şevin Turcan

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Microenvironmental Drivers of Glioma Progression.International journal of molecular sciences · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Metabolic Rewiring in Adult-Type Diffuse Gliomas.International journal of molecular sciences · 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

7 authors at 3 institutions in 2 countries.

Jong-Whi ParkNeurology Clinic and National Center for Tumor Diseases, University Hospital Heidelberg, INF 460, 69120, Heidelberg, Germany. jpark@gachon.ac.kr.ORCID 0000-0002-9890-9241
Omer KilicNeurology Clinic and National Center for Tumor Diseases, University Hospital Heidelberg, INF 460, 69120, Heidelberg, Germany.
Minh DeoNeurology Clinic and National Center for Tumor Diseases, University Hospital Heidelberg, INF 460, 69120, Heidelberg, Germany.
Kevin Jimenez-CowellNeurology Clinic and National Center for Tumor Diseases, University Hospital Heidelberg, INF 460, 69120, Heidelberg, Germany.
Engin DemirdizenNeurology Clinic and National Center for Tumor Diseases, University Hospital Heidelberg, INF 460, 69120, Heidelberg, Germany.
Hyunggee KimDepartment of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, South Korea.
Şevin TurcanNeurology Clinic and National Center for Tumor Diseases, University Hospital Heidelberg, INF 460, 69120, Heidelberg, Germany. sevin.turcan@med.uni-heidelberg.de.ORCID 0000-0002-0885-5607
Heidelberg University · DEGachon University · KRKorea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Capicua (CIC) is an important downstream molecule of RTK/RAS/MAPK pathway. The regulatory mechanism of CIC underlying tumorigenesis in oligodendroglioma, where CIC is frequently mutated, has yet to be fully elucidated. Using patient-derived glioma lines, RNA-sequencing and bioinformatic analysis of publicly available databases, we investigated how CIC loss- or gain-of-function regulates its downstream targets, cell proliferation and glutamate release. Our results indicate an increased frequency of CIC truncating mutations in oligodendroglioma during progression. In vitro, CIC modulation had a modest effect on cell proliferation in glioma lines, and no significant changes in the expression of ETV1, ETV4 and ETV5. Transcriptional repression of known CIC targets was observed in gliomas expressing non-phosphorylatable CIC variant on Ser173 which was unable to interact with 14-3-3. These data outline a mechanism by which the repressor function of CIC is inhibited by 14-3-3 in gliomas. Using transcriptional profiling, we found that genes related to glutamate release were upregulated because of CIC depletion. In addition, loss of CIC leads to increased extracellular glutamate. Consistent with this, CIC restoration in an oligodendroglioma line reduced the levels of extracellular glutamate, neuronal toxicity and xCT/SLC7A11 expression. Our findings may provide a molecular basis for the prevention of glioma-associated seizures.

Indexed as

Amino Acid Transport System y+GliomaOligodendrogliomaRepressor ProteinsGlutamic AcidHumansNeuronsAmino Acid Transport System y+CIC protein, humanGlutamic AcidRepressor ProteinsSLC7A11 protein, humanCapicuaGlutamateNeuronal toxicityOligodendrogliomaxCT/SLC7A11

Identifiers

PMID36647117
PMCPMC9843885
OpenAlexW4316663007

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.