Evidence map›Paper›PMID 38986826›Full record

ArticleBiochimica et biophysica acta. Bioenergetics2024

Differential regulation of mitochondrial uncoupling protein 2 in cancer cells.

Taraneh Beikbaghban, Ludovica Proietti, Jessica Ebner, Roko Sango, Thomas Rattei, Thomas Weichhart, Florian Grebien, Felix Sternberg, Elena E Pohl

Abstract read
In one paragraph

Article in Biochimica et biophysica acta. Bioenergetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Deciphering Uncoupling Proteins in Cellular Homeostasis and Metabolic Health.International journal of biological sciences · 2026
    Review
  4. Article
  5. Article
  6. Article
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

9 authors.

Taraneh BeikbaghbanPhysiology and Biophysics, Department of Biological Sciences and Pathobiology, University of Veterinary Medicine, Vienna, Austria.
Ludovica ProiettiInstitute for Medical Biochemistry, University of Veterinary Medicine, Vienna, Austria.
Jessica EbnerInstitute for Medical Biochemistry, University of Veterinary Medicine, Vienna, Austria.
Roko SangoCentre for Microbiology and Environmental Systems Science, University of Vienna, Vienna, Austria; Center of Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Vienna, Austria; Doctoral School in Microbiology and Environmental Science, University of Vienna, Vienna, Austria.
Thomas RatteiCentre for Microbiology and Environmental Systems Science, University of Vienna, Vienna, Austria.
Thomas WeichhartCenter of Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Austria.
Florian GrebienInstitute for Medical Biochemistry, University of Veterinary Medicine, Vienna, Austria; St. Anna Children's Cancer Research Institute (CCRI), Vienna, Austria; CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Felix SternbergPhysiology and Biophysics, Department of Biological Sciences and Pathobiology, University of Veterinary Medicine, Vienna, Austria; Department of Nutritional Sciences, Faculty of Life Sciences, University of Vienna, Austria. Electronic address: felix.sternberg@univie.ac.at.
Elena E PohlPhysiology and Biophysics, Department of Biological Sciences and Pathobiology, University of Veterinary Medicine, Vienna, Austria. Electronic address: elena.pohl@vetmeduni.ac.at.

Funding

Austrian Science Fund FWF F 8305
6 · The paper itself

Abstract

The persistent growth of cancer cells is underscored by complex metabolic reprogramming, with mitochondria playing a key role in the transition to aerobic glycolysis and representing new therapeutic targets. Mitochondrial uncoupling protein 2 (UCP2) has attracted interest because of its abundance in rapidly proliferating cells, including cancer cells, and its involvement in cellular metabolism. However, the specific contributions of UCP2 to cancer biology remain poorly defined. Our investigation of UCP2 expression in various human and mouse cancer cell lines aimed to elucidate its links to metabolic states, proliferation, and adaptation to environmental stresses such as hypoxia and nutrient deprivation. We observed significant variability in UCP2 expression across cancer types, with no direct correlation to their metabolic activity or proliferation rates. UCP2 abundance was also differentially affected by nutrient availability in different cancer cells, but UCP2 was generally downregulated under hypoxia. These findings challenge the notion that UCP2 is a marker of malignant potential and suggest its more complex involvement in the metabolic landscape of cancer.

Indexed as

NeoplasmsUncoupling Protein 2AnimalsCell HypoxiaCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceMitochondriaUCP2 protein, humanUcp2 protein, mouseUncoupling Protein 2Citric acid cycleExtracellular acidification rateMetabolite transportOxygen consumption ratePyruvate kinaseUncouplersWarburg effect

Identifiers

PMID38986826
PMCPMC7617651

What OpenQuestion 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 OpenQuestion graph.