Evidence map›Paper›PMID 29248131›Full record

ReviewSeminars in oncology2017

Metabolic coupling and the Reverse Warburg Effect in cancer: Implications for novel biomarker and anticancer agent development.

Lindsay Wilde, Megan Roche, Marina Domingo-Vidal, Katherina Tanson, Nancy Philp, Joseph Curry, Ubaldo Martinez-Outschoorn

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers.

0numbers the graph read from it
0cells of the map it votes in
200citing papers in PubMed
8.5field-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

200 citing papers in PubMed, 314 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. The Application of 3D Cell Culture in Thyroid Cancer.Annals of biomedical engineering · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Fraternal cooperation of hierarchical cancer parallels metazoan multicellularity and eusociality.Biological reviews of the Cambridge Philosophical Society · 2026
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Lactate and lactylation in tumor immunity.Frontiers of medicine · 2025
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Review

140 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

7 authors at 2 institutions in 1 country.

Lindsay WildeDepartment of Medical Oncology Thomas Jefferson University, Philadelphia, PA.
Megan RocheDepartment of Medical Oncology Thomas Jefferson University, Philadelphia, PA.
Marina Domingo-VidalDepartment of Medical Oncology Thomas Jefferson University, Philadelphia, PA.
Katherina TansonDrexel University, Philadelphia, PA.
Nancy PhilpDepartment of Cell Biology, Anatomy and Pathology, Thomas Jefferson University, Philadelphia, PA.
Joseph CurryDepartment of Otolaryngology, Thomas Jefferson University, Philadelphia, PA.
Ubaldo Martinez-OutschoornDepartment of Medical Oncology Thomas Jefferson University, Philadelphia, PA. Electronic address: ubaldo.martinez-outschoorn@jefferson.edu.
Thomas Jefferson University · USDrexel University · US

Funding

Metabolic mechanisms of antiestrogen resistance in breast cancerK08CA175193 · NCI · THOMAS JEFFERSON UNIVERSITY · PI MARTINEZ OUTSCHOORN, UBALDO · 2013 to 2017
$831k
NCI NIH HHS K08 CA175193
6 · The paper itself

Abstract

Glucose is a key metabolite used by cancer cells to generate ATP, maintain redox state and create biomass. Glucose can be catabolized to lactate in the cytoplasm, which is termed glycolysis, or alternatively can be catabolized to carbon dioxide and water in the mitochondria via oxidative phosphorylation. Metabolic heterogeneity exists in a subset of human tumors, with some cells maintaining a glycolytic phenotype while others predominantly utilize oxidative phosphorylation. Cells within tumors interact metabolically with transfer of catabolites from supporting stromal cells to adjacent cancer cells. The Reverse Warburg Effect describes when glycolysis in the cancer-associated stroma metabolically supports adjacent cancer cells. This catabolite transfer, which induces stromal-cancer metabolic coupling, allows cancer cells to generate ATP, increase proliferation, and reduce cell death. Catabolites implicated in metabolic coupling include the monocarboxylates lactate, pyruvate, and ketone bodies. Monocarboxylate transporters (MCT) are critically necessary for release and uptake of these catabolites. MCT4 is involved in the release of monocarboxylates from cells, is regulated by catabolic transcription factors such as hypoxia inducible factor 1 alpha (HIF1A) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and is highly expressed in cancer-associated fibroblasts. Conversely, MCT1 is predominantly involved in the uptake of these catabolites and is highly expressed in a subgroup of cancer cells. MYC and TIGAR, which are genes involved in cellular proliferation and anabolism, are inducers of MCT1. Profiling human tumors on the basis of an altered redox balance and intra-tumoral metabolic interactions may have important biomarker and therapeutic implications. Alterations in the redox state and mitochondrial function of cells can induce metabolic coupling. Hence, there is interest in redox and metabolic modulators as anticancer agents. Also, markers of metabolic coupling have been associated with poor outcomes in numerous human malignancies and may be useful prognostic and predictive biomarkers.

Indexed as

Adenosine TriphosphateAntineoplastic AgentsApoptosis Regulatory ProteinsCell ProliferationDrug DiscoveryFibroblastsGlucoseGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitIntracellular Signaling Peptides and ProteinsKetone BodiesLactic AcidMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersMuscle ProteinsAdenosine TriphosphateAntineoplastic AgentsApoptosis Regulatory ProteinsGlucoseHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitIntracellular Signaling Peptides and ProteinsKetone BodiesLactic AcidMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersMuscle ProteinsMYC protein, humanNF-kappa BPhosphoric Monoester HydrolasesProto-Oncogene Proteins c-mycPyruvic AcidSLC16A4 protein, humanSymportersTIGAR protein, humancaveolin 1glycolysishypoxia inducible factorlactateoxidative phosphorylationTIGAR

Identifiers

PMID29248131
PMCPMC5737780
OpenAlexW2763966161

What OpenQuestion holds

Textmetadata
LicenceTDM
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.