Evidence map›Paper›PMID 30487597›Full record

ReviewOncogene2019

The ERK and JNK pathways in the regulation of metabolic reprogramming.

Salvatore Papa, Pui Man Choy, Concetta Bubici

Open access · hybridAbstract readReview
In one paragraph

Review in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 238 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
238citing papers in PubMed, 2 pooled it
11.4field-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

238 citing papers in PubMed, 2 syntheses or guidelines pooled it, 402 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. The Dynamic Alliance of p53 and Metabolism in the Tumor Microenvironment Shapes Tumor Evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
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  20. Metabolic stress conditions dictate MAPKAPK2-dependent efficiency of MEK1/2 inhibition in colorectal carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article

178 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 2 institutions in 1 country.

Salvatore PapaCell Signaling and Cancer Laboratory, Leeds Institute of Cancer and Pathology, Faculty of Medicine and Health, University of Leeds, St James' University Hospital, Beckett Street, Leeds, UK. s.papa@leeds.ac.uk.ORCID http://orcid.org/0000-0002-8369-6538
Pui Man ChoyCell Signaling and Cancer Laboratory, Leeds Institute of Cancer and Pathology, Faculty of Medicine and Health, University of Leeds, St James' University Hospital, Beckett Street, Leeds, UK.
Concetta BubiciCollege of Health and Life Sciences, Department of Life Sciences, Institute of Environment, Health and Societies, Division of Biosciences, Brunel University London, Uxbridge, UK. concetta.bubici@brunel.ac.uk.ORCID http://orcid.org/0000-0002-8074-4661
University of Leeds · GBImperial College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most tumor cells reprogram their glucose metabolism as a result of mutations in oncogenes and tumor suppressors, leading to the constitutive activation of signaling pathways involved in cell growth. This metabolic reprogramming, known as aerobic glycolysis or the Warburg effect, allows tumor cells to sustain their fast proliferation and evade apoptosis. Interfering with oncogenic signaling pathways that regulate the Warburg effect in cancer cells has therefore become an attractive anticancer strategy. However, evidence for the occurrence of the Warburg effect in physiological processes has also been documented. As such, close consideration of which signaling pathways are beneficial targets and the effect of their inhibition on physiological processes are essential. The MAPK/ERK and MAPK/JNK pathways, crucial for normal cellular responses to extracellular stimuli, have recently emerged as key regulators of the Warburg effect during tumorigenesis and normal cellular functions. In this review, we summarize our current understanding of the roles of the ERK and JNK pathways in controlling the Warburg effect in cancer and discuss their implication in controlling this metabolic reprogramming in physiological processes and opportunities for targeting their downstream effectors for therapeutic purposes.

Indexed as

AnimalsCell Transformation, NeoplasticCellular ReprogrammingEnergy MetabolismGlycolysisHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemNeoplasmsJNK Mitogen-Activated Protein Kinases

Identifiers

PMID30487597
PMCPMC6398583
OpenAlexW2902532424

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.