Evidence map›Paper›PMID 31530011›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2019

IDH2 reprograms mitochondrial dynamics in cancer through a HIF-1α

Yuan Wang, Ekta Agarwal, Irene Bertolini, Jagadish C Ghosh, Jae Ho Seo, Dario C Altieri

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Histopathologic and Molecular Characterization of IDH-Mutant Prostatic Adenocarcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2025
    Article
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  9. Article
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  11. Review
  12. Article
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  15. Article
  16. MicroRNA 101 Attenuated NSCLC Proliferation through IDH2/HIFOxidative medicine and cellular longevity · 2022
    Article
  17. Mitochondrial Fission and Fusion in Tumor Progression to Metastasis.Frontiers in cell and developmental biology · 2022
    Review
  18. Review
  19. Review
  20. 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

6 authors at 1 institution in 1 country.

Yuan WangThe Wistar Institute, Philadelphia, Pennsylvania, USA.
Ekta AgarwalThe Wistar Institute, Philadelphia, Pennsylvania, USA.
Irene BertoliniThe Wistar Institute, Philadelphia, Pennsylvania, USA.
Jagadish C GhoshThe Wistar Institute, Philadelphia, Pennsylvania, USA.
Jae Ho SeoThe Wistar Institute, Philadelphia, Pennsylvania, USA.
Dario C AltieriThe Wistar Institute, Philadelphia, Pennsylvania, USA.
The Wistar Institute · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
Role of Runx2 in prostate tumorigenesis and metastasisP01CA140043 · NCI · WISTAR INSTITUTE · PI ALTIERI, DARIO C · 2010 to 2021
$12.2M
Tumor PlasticityR35CA220446 · NCI · WISTAR INSTITUTE · PI ALTIERI, DARIO C · 2017 to 2023
$7.7M
NCI NIH HHS P01 CA140043NCI NIH HHS P30 CA010815NCI NIH HHS R35 CA220446
6 · The paper itself

Abstract

The role of mitochondria in cancer continues to be debated and paradoxically implicated in opposing functions in tumor growth and tumor suppression. To understand this dichotomy, we explored the function of mitochondrial isocitrate dehydrogenase (IDH)2, a tricarboxylic acid cycle enzyme mutated in subsets of acute leukemias and gliomas, in cancer. Silencing of IDH2 in prostate cancer cells impaired oxidative bioenergetics, elevated reactive oxygen species (ROS) production, and promoted exaggerated mitochondrial dynamics. This was associated with increased subcellular mitochondrial trafficking, turnover of membrane focal adhesion complexes, and enhanced tumor cell migration and invasion, without changes in cell cycle progression. Mechanistically, loss of IDH2 caused ROS-dependent stabilization of hypoxia-inducible factor-1α in normoxia, which was required for increased mitochondrial trafficking and tumor cell movements. Therefore, IDH2 is a dual regulator of cancer bioenergetics and tumor cell motility. This pathway may reprogram mitochondrial dynamics to differentially adjust energy production or promote tumor cell invasion in response to microenvironment conditions.-Wang, Y., Agarwal, E., Bertolini, I., Ghosh, J. C., Seo, J. H., Altieri, D. C. IDH2 reprograms mitochondrial dynamics in cancer through a HIF-1α-regulated pseudohypoxic state.

Indexed as

Energy MetabolismMitochondrial DynamicsAnimalsApoptosisCell MovementCell ProliferationHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitIsocitrate DehydrogenaseMaleMiceMitochondriaOxidation-ReductionProstatic NeoplasmsReactive Oxygen SpeciesHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitIDH2 protein, humanIsocitrate DehydrogenaseReactive Oxygen SpeciesHIF-1α metastasismitochondriaROStumor cell motility

Identifiers

PMID31530011
PMCPMC6894043
OpenAlexW2974269991

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.