Evidence map›Paper›PMID 25531325›Full record

ArticleOncogene2015

Aberrant IDH3α expression promotes malignant tumor growth by inducing HIF-1-mediated metabolic reprogramming and angiogenesis.

L Zeng, A Morinibu, M Kobayashi, Y Zhu, X Wang, Y Goto, C J Yeom, T Zhao, K Hirota, K Shinomiya and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

63 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Revealing the Role of Beesioside O fromInternational journal of molecular sciences · 2025
    Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

3 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

16 authors at 4 institutions in 3 countries.

L ZengDepartment of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine, Kyoto, Japan.
A MorinibuDepartment of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine, Kyoto, Japan.
M KobayashiDepartment of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Y ZhuDepartment of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine, Kyoto, Japan.
X WangDepartment of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Y GotoDepartment of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine, Kyoto, Japan.
C J YeomGroup of Radiation and Tumor Biology, Career-Path Promotion Unit for Young Life Scientists, Kyoto University, Yoshida Konoe-cho, Kyoto, Japan.
T ZhaoDepartment of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine, Kyoto, Japan.
K HirotaDepartment of Anesthesia, Kyoto University Hospital, Kyoto University, Kyoto, Japan.
K ShinomiyaDepartment of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine, Kyoto, Japan.
S ItasakaDepartment of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine, Kyoto, Japan.
M YoshimuraDepartment of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine, Kyoto, Japan.
G GuoDepartment of Radiation Medicine, Fourth Military Medical University, Shaanxi, China.
E M HammondDepartment of Oncology, Oxford Institute for Radiation Oncology, University of Oxford, Oxford, UK.
M HiraokaDepartment of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine, Kyoto, Japan.
H HaradaDepartment of Radiation Oncology and Image-applied Therapy, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kyoto University · JPAir Force Medical University · CNKyoto University Hospital · JPUniversity of Oxford · GB

Funding

Cancer Research UK 19276
6 · The paper itself

Abstract

Cancer cells gain a growth advantage through the so-called Warburg effect by shifting glucose metabolism from oxidative phosphorylation to aerobic glycolysis. Hypoxia-inducible factor 1 (HIF-1) has been suggested to function in metabolic reprogramming; however, the underlying mechanism has not been fully elucidated. We found that the aberrant expression of wild-type isocitrate dehydrogenase 3α (IDH3α), a subunit of the IDH3 heterotetramer, decreased α-ketoglutarate levels and increased the stability and transactivation activity of HIF-1α in cancer cells. The silencing of IDH3α significantly delayed tumor growth by suppressing the HIF-1-mediated Warburg effect and angiogenesis. IDH3α expression was associated with the poor postoperative overall survival of lung and breast cancer patients. These results justify the exploitation of IDH3 as a novel target for the diagnosis and treatment of cancers.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticGlucoseGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitIsocitrate DehydrogenaseLung NeoplasmsMiceNeovascularization, PathologicOxidative PhosphorylationGlucoseHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitIsocitrate Dehydrogenase

Identifiers

PMID25531325
OpenAlexW2060817767

What OpenQuestion holds

Textmetadata
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.