Evidence map›Paper›PMID 24036851›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2013

Targeting protein kinase CK2 suppresses prosurvival signaling pathways and growth of glioblastoma.

Ying Zheng, Braden C McFarland, Denis Drygin, Hao Yu, Susan L Bellis, Hyunsoo Kim, Markus Bredel, Etty N Benveniste

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

81 citing papers in PubMed, 138 citations in OpenAlex.

  1. Article
  2. Review
  3. Silmitasertib, an FDA-designated orphan CK2 inhibitor, ameliorates neuropathology and motor dysfunction in a Huntington's disease mouse model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. CK2 Chemical Probes: Past, Present, and Future.Kinases and phosphatases · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Protein Kinase CK2 Controls CD8Journal of immunology (Baltimore, Md. : 1950) · 2022
    Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Ying ZhengAuthors' Affiliations: Departments of Cell, Developmental and Integrative Biology, Pathology, and Radiation Oncology, University of Alabama at Birmingham, Birmingham, Alabama; and Cylene Pharmaceuticals, San Diego, California.
Braden C McFarland
Denis Drygin
Hao Yu
Susan L Bellis
Hyunsoo Kim
Markus Bredel
Etty N Benveniste
University of Alabama at Birmingham · US

Funding

UAB Neuroscience Core CenterP30NS047466 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STANDAERT, DAVID G. · 2005 to 2019
$8.5M
Targeting the JAK/STAT-3 Pathway Signaling Axis in GliomaR01CA158534 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENVENISTE, ETTY N · 2012 to 2016
$1.5M
NCI NIH HHS R01 CA158534NINDS NIH HHS P30 NS047466
6 · The paper itself

Abstract

purposeGliomas are the most frequently occurring primary malignancies in the brain, and glioblastoma is the most aggressive of these tumors. Protein kinase CK2 is composed of two catalytic subunits (α and/or α') and two β regulatory subunits. CK2 suppresses apoptosis, promotes neoangiogenesis, and enhances activation of the JAK/STAT, NF-κB, PI3K/AKT, Hsp90, Wnt, and Hedgehog pathways. Aberrant activation of the NF-κB, PI3K/AKT, and JAK/STAT-3 pathways is implicated in glioblastoma progression. As CK2 is involved in their activation, the expression and function of CK2 in glioblastoma was evaluated. EXPERIMENTAL DESIGN AND

resultsAnalysis of 537 glioblastomas from The Cancer Genome Atlas Project demonstrates the CSNK2A1 gene, encoding CK2α, has gene dosage gains in glioblastoma (33.7%), and is significantly associated with the classical glioblastoma subtype. Inhibition of CK2 activity by CX-4945, a selective CK2 inhibitor, or CK2 knockdown by siRNA suppresses activation of the JAK/STAT, NF-κB, and AKT pathways and downstream gene expression in human glioblastoma xenografts. On a functional level, CX-4945 treatment decreases the adhesion and migration of glioblastoma cells, in part through inhibition of integrin β1 and α4 expression. In vivo, CX-4945 inhibits activation of STAT-3, NF-κB p65, and AKT, and promotes survival of mice with intracranial human glioblastoma xenografts.

conclusionsCK2 inhibitors may be considered for treatment of patients with glioblastoma.

Indexed as

Signal TransductionAnimalsAntineoplastic AgentsBrain NeoplasmsCasein Kinase IICell AdhesionCell Line, TumorCell MovementCell ProliferationCell SurvivalEnzyme ActivationFemaleGene AmplificationGene DosageGlioblastomaHumansAntineoplastic AgentsCasein Kinase IICSNK2A1 protein, humanNaphthyridinesPhenazinesProto-Oncogene Proteins c-aktsilmitasertibSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID24036851
PMCPMC3932633
OpenAlexW2125248088

What OpenQuestion holds

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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.