Evidence map›Paper›PMID 29478262›Full record

ReviewCancer science2018

Roles of protein kinase R in cancer: Potential as a therapeutic target.

Takao Watanabe, Takeshi Imamura, Yoichi Hiasa

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Sterile activation of RNA-sensing pathways in autoimmunity.Journal of molecular cell biology · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Propofol Induces the Expression of Nrf2 and HO-1 inTropical medicine and infectious disease · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Oocyte age and preconceptual alcohol use are highly correlated with epigenetic imprinting of a noncoding RNA (Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Takao WatanabeDepartment of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Toon, Japan.ORCID http://orcid.org/0000-0002-7929-1781
Takeshi ImamuraDepartment of Molecular Medicine for Pathogenesis, Ehime University Graduate School of Medicine, Toon, Ehime, Japan.ORCID http://orcid.org/0000-0001-5101-4304
Yoichi HiasaDepartment of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Toon, Japan.ORCID http://orcid.org/0000-0003-4117-339X
Ehime University · JPEhime University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Double-stranded (ds) RNA-dependent protein kinase (PKR) is a ubiquitously expressed serine/threonine protein kinase. It was initially identified as an innate immune antiviral protein induced by interferon (IFN) and activated by dsRNA. PKR is recognized as a key executor of antiviral host defense. Moreover, it contributes to inflammation and immune regulation through several signaling pathways. In addition to IFN and dsRNA, PKR is activated by multiple stimuli and regulates various signaling pathways including the mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells pathways. PKR was initially thought to be a tumor suppressor as a result of its ability to suppress cell growth and interact with major tumor suppressor genes. However, in several types of malignant disease, such as colon and breast cancers, its role remains controversial. In hepatocellular carcinoma, hepatitis C virus (HCV) is the main cause of liver cancer, and PKR inhibits HCV replication, indicating its role as a tumor suppressor. However, PKR is overexpressed in cirrhotic patients, and acts as a tumor promoter through enhancement of cancer cell growth by mediating MAPK or signal transducer and activator of transcription pathways. Moreover, PKR is reportedly required for the activation of inflammasomes and influences metabolic disorders. In the present review, we introduce the multifaceted roles of PKR such as antiviral function, tumor cell growth, regulation of inflammatory immune responses, and maintaining metabolic homeostasis; and discuss future perspectives on PKR biology including its potential as a therapeutic target for liver cancer.

Indexed as

AnimalseIF-2 KinaseHumansInflammationLiver NeoplasmsMitogen-Activated Protein KinasesProtein Serine-Threonine KinaseseIF-2 KinaseMitogen-Activated Protein KinasesProtein Serine-Threonine Kinasesdouble-stranded (ds) RNA-dependent protein kinase (PKR)hepatitis C virus (HCV)hepatocellular carcinoma (HCC)interferonmitogen-activated protein kinase (MAPK)

Identifiers

PMID29478262
PMCPMC5891186
OpenAlexW2791830191

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.