Evidence map›Paper›PMID 34685488›Full record

ReviewCells2021

ERK: A Double-Edged Sword in Cancer. ERK-Dependent Apoptosis as a Potential Therapeutic Strategy for Cancer.

Reiko Sugiura, Ryosuke Satoh, Teruaki Takasaki

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 212 papers.

0numbers the graph read from it
0cells of the map it votes in
212citing papers in PubMed
16.1field-weighted citation impact, top 1% 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

212 citing papers in PubMed, 328 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Unveiling the Role of GlutathioneACS pharmacology & translational science · 2026
    Review
  8. ERK autoinhibition mechanism informs a drug combination strategy.Protein science : a publication of the Protein Society · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Targeting WNK1 Releases Differentiation Block in Acute Myeloid Leukemia.bioRxiv : the preprint server for biology · 2026
    Article
  17. Article
  18. Article
  19. Review
  20. TargetingJournal of Zhejiang University. Science. B · 2026
    Article

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

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 1 institution in 1 country.

Reiko SugiuraLaboratory of Molecular Pharmacogenomics, Department of Pharmaceutical Sciences, Faculty of Pharmacy, Kindai University, Osaka 577-8502, Japan.ORCID 0000-0001-6946-0935
Ryosuke SatohLaboratory of Molecular Pharmacogenomics, Department of Pharmaceutical Sciences, Faculty of Pharmacy, Kindai University, Osaka 577-8502, Japan.
Teruaki TakasakiLaboratory of Molecular Pharmacogenomics, Department of Pharmaceutical Sciences, Faculty of Pharmacy, Kindai University, Osaka 577-8502, Japan.ORCID 0000-0002-7670-1896
Kindai University · JP

Funding

Japan Society for the Promotion of Science JP19H03376Ministry of Education, Culture, Sports, Science and Technology JPS1411037
6 · The paper itself

Abstract

The RAF/MEK/ERK signaling pathway regulates diverse cellular processes as exemplified by cell proliferation, differentiation, motility, and survival. Activation of ERK1/2 generally promotes cell proliferation, and its deregulated activity is a hallmark of many cancers. Therefore, components and regulators of the ERK pathway are considered potential therapeutic targets for cancer, and inhibitors of this pathway, including some MEK and BRAF inhibitors, are already being used in the clinic. Notably, ERK1/2 kinases also have pro-apoptotic functions under certain conditions and enhanced ERK1/2 signaling can cause tumor cell death. Although the repertoire of the compounds which mediate ERK activation and apoptosis is expanding, and various anti-cancer compounds induce ERK activation while exerting their anti-proliferative effects, the mechanisms underlying ERK1/2-mediated cell death are still vague. Recent studies highlight the importance of dual-specificity phosphatases (DUSPs) in determining the pro- versus anti-apoptotic function of ERK in cancer. In this review, we will summarize the recent major findings in understanding the role of ERK in apoptosis, focusing on the major compounds mediating ERK-dependent apoptosis. Studies that further define the molecular targets of these compounds relevant to cell death will be essential to harnessing these compounds for developing effective cancer treatments.

Indexed as

ApoptosisDual-Specificity PhosphatasesHumansMAP Kinase Signaling SystemNeoplasmsProtein Kinase InhibitorsSignal TransductionDual-Specificity PhosphatasesProtein Kinase InhibitorsACA-28apoptosiscancer treatmentDUSP/MKPRAS/RAF/MEK/ERK signaling

Identifiers

PMID34685488
PMCPMC8533760
OpenAlexW3199076451

What Socratic 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 Socratic graph.