Evidence map›Paper›PMID 30206363›Full record

ArticleScientific reports2018

Casein Kinase 1 Epsilon Regulates Glioblastoma Cell Survival.

Robin T Varghese, Sarah Young, Lily Pham, Yanping Liang, Kevin J Pridham, Sujuan Guo, Susan Murphy, Deborah F Kelly, Zhi Sheng

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Casein kinase 1α mediates eryptosis: a review.Apoptosis : an international journal on programmed cell death · 2023
    Review
  5. Review
  6. Article
  7. Article
  8. Wnt/β-catenin signaling in cancers and targeted therapies.Signal transduction and targeted therapy · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. GLI3: a mediator of genetic diseases, development and cancer.Cell communication and signaling : CCS · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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

9 authors at 2 institutions in 1 country.

Robin T VargheseVirginia Tech Carilion Research Institute, Roanoke, VA, 24016, United States.
Sarah YoungVirginia Tech Carilion Research Institute, Roanoke, VA, 24016, United States.
Lily PhamVirginia Tech Carilion Research Institute, Roanoke, VA, 24016, United States.
Yanping LiangVirginia Tech Carilion Research Institute, Roanoke, VA, 24016, United States.
Kevin J PridhamVirginia Tech Carilion Research Institute, Roanoke, VA, 24016, United States.
Sujuan GuoVirginia Tech Carilion Research Institute, Roanoke, VA, 24016, United States.
Susan MurphyVirginia Tech Carilion Research Institute, Roanoke, VA, 24016, United States.
Deborah F KellyVirginia Tech Carilion Research Institute, Roanoke, VA, 24016, United States.
Zhi ShengVirginia Tech Carilion Research Institute, Roanoke, VA, 24016, United States. zhisheng@vtc.vt.edu.
Virginia Tech · USCarilion Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma is the most common malignant brain cancer with a dismal prognosis. The difficulty in treating glioblastoma is largely attributed to the lack of effective therapeutic targets. In our previous work, we identified casein kinase 1 ε (CK1ε, also known as CSNK1E) as a potential survival factor in glioblastoma. However, how CK1ε controls cell survival remains elusive and whether targeting CK1ε is a possible treatment for glioblastoma requires further investigation. Here we report that CK1ε was expressed at the highest level among six CK1 isoforms in glioblastoma and enriched in high-grade glioma, but not glia cells. Depletion of CK1ε remarkably inhibited the growth of glioblastoma cells and suppressed self-renewal of glioblastoma stem cells, while having limited effect on astrocytes. CK1ε deprivation activated β-catenin and induced apoptosis, which was further counteracted by knockdown of β-catenin. The CK1ε inhibitor IC261, but not PF-4800567, activated β-catenin and blocked the growth of glioblastoma cells and glioblastoma stem cells. Congruently, IC261 elicited a robust growth inhibition of human glioblastoma xenografts in mice. Together, our results demonstrate that CK1ε regulates the survival of glioblastoma cells and glioblastoma stem cells through β-catenin signaling, underscoring the importance of targeting CK1ε as an effective treatment for glioblastoma.

Indexed as

Signal TransductionAnimalsbeta CateninCasein Kinase ICell Line, TumorCell SurvivalGlioblastomaHumansIndolesIsoenzymesMiceMice, Inbred BALB CMice, NudeNeoplasm ProteinsPhloroglucinolPyrazoles3-(3-chlorophenoxymethyl)-1-(tetrahydropyran-4-yl)-1H-pyrazolo(3,4-d)pyrimidin-4-ylaminebeta CateninCasein Kinase IIC 261IndolesIsoenzymesNeoplasm ProteinsPhloroglucinolPyrazolesPyrimidines

Identifiers

PMID30206363
PMCPMC6134061
OpenAlexW2889687626

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.