Evidence map›Paper›PMID 36114992›Full record

ReviewMolecular and cellular biochemistry2023

Protein kinase CK2 - diverse roles in cancer cell biology and therapeutic promise.

Janeen H Trembley, Betsy T Kren, Muhammad Afzal, George A Scaria, Mark A Klein, Khalil Ahmed

Erratum issuedOpen access · bronzeAbstract readReview
In one paragraph

Review in Molecular and cellular biochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Tyrosine kinases sample unique activation ensembles.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. CK2B Induces CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Janeen H TrembleyResearch Service, Minneapolis VA Health Care System, Minneapolis, MN, 55417, USA. trem0005@umn.edu.ORCID http://orcid.org/0000-0003-3597-2611
Betsy T KrenResearch Service, Minneapolis VA Health Care System, Minneapolis, MN, 55417, USA.
Muhammad AfzalDepartment of Biochemistry, Riphah International University, Islamabad, Pakistan.ORCID http://orcid.org/0000-0002-5785-6067
George A ScariaHematology/Oncology Section, Primary Care Service Line, Minneapolis VA Health Care System, Minneapolis, MN, 55417, USA.
Mark A KleinMasonic Cancer Center, University of Minnesota, Minneapolis, MN, 55455, USA.
Khalil AhmedResearch Service, Minneapolis VA Health Care System, Minneapolis, MN, 55417, USA. ahmedk@umn.edu.ORCID http://orcid.org/0000-0003-4531-6837
University of Minnesota · USMinneapolis VA Health Care System · USRiphah International University · PK

Funding

A Novel Therapeutic Approach for Primary and Metastatic Prostate CancerR01CA150182 · NCI · UNIVERSITY OF MINNESOTA · PI AHMED, KHALIL · 2011 to 2015
$1.4M
STUDIES OF NORMAL AND NEOPLASTIC PROSTATER01CA015062 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI AHMED, KHALIL · 1985 to 2002
$578k
Mechanisms of CK2-regulated prostate cancer survival and deathI01BX003282 · VA · MINNEAPOLIS VA MEDICAL CENTER · PI AHMED, KHALIL · 2016 to 2019
–
Dynamics of protein kinase CK2 signaling in prostate cancer pathogenesisI01BX005091 · VA · MINNEAPOLIS VA MEDICAL CENTER · PI AHMED, KHALIL · 2021 to 2024
–
BLRD VA I01 BX003282BLRD VA I01 BX005091National Cancer Institute, NIH, Department of Health and Human Services RO1CA15062NCI NIH HHS R01 CA015062NCI NIH HHS R01 CA150182
6 · The paper itself

Abstract

The association of protein kinase CK2 (formerly casein kinase II or 2) with cell growth and proliferation in cells was apparent at early stages of its investigation. A cancer-specific role for CK2 remained unclear until it was determined that CK2 was also a potent suppressor of cell death (apoptosis); the latter characteristic differentiated its function in normal versus malignant cells because dysregulation of both cell growth and cell death is a universal feature of cancer cells. Over time, it became evident that CK2 exerts its influence on a diverse range of cell functions in normal as well as in transformed cells. As such, CK2 and its substrates are localized in various compartments of the cell. The dysregulation of CK2 is documented in a wide range of malignancies; notably, by increased CK2 protein and activity levels with relatively moderate change in its RNA abundance. High levels of CK2 are associated with poor prognosis in multiple cancer types, and CK2 is a target for active research and testing for cancer therapy. Aspects of CK2 cellular roles and targeting in cancer are discussed in the present review, with focus on nuclear and mitochondrial functions and prostate, breast and head and neck malignancies.

Indexed as

Casein Kinase IIHead and Neck NeoplasmsApoptosisCell DeathCell NucleusHumansMaleCasein Kinase IIApoptosisCancerCancer therapyCell deathChromatinIntracellular shuttlingMitochondriaNuclear matrixNucleolusNucleusProgressionProtein kinase CK2SplicingTranscription

Identifiers

PMID36114992
PMCPMC9483426
OpenAlexW4296120037

What OpenQuestion holds

Textmetadata
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.