Evidence map›Paper›PMID 24351290›Full record

ArticleCancer research2014

Cysteine catabolism: a novel metabolic pathway contributing to glioblastoma growth.

Antony Prabhu, Bhaswati Sarcar, Soumen Kahali, Zhigang Yuan, Joseph J Johnson, Klaus-Peter Adam, Elizabeth Kensicki, Prakash Chinnaiyan

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

60 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
  2. SQOR regulates HResearch square · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Cysteine induces mitochondrial reductive stress in glioblastoma through hydrogen peroxide production.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  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

8 authors at 2 institutions in 1 country.

Antony PrabhuAuthors' Affiliations: Radiation Oncology; Chemical Biology and Molecular Medicine; Advanced Microscopy Laboratory; Cancer Imaging and Metabolism, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida; and Metabolon, Inc., Durham, North Carolina.
Bhaswati Sarcar
Soumen Kahali
Zhigang Yuan
Joseph J Johnson
Klaus-Peter Adam
Elizabeth Kensicki
Prakash Chinnaiyan
Moffitt Cancer Center · USMetabolon (United States) · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI John L. Cleveland · 1998 to 2026
$93.5M
NCI NIH HHS P30 CA076292
6 · The paper itself

Abstract

The relevance of cysteine metabolism in cancer has gained considerable interest in recent years, largely focusing on its role in generating the antioxidant glutathione. Through metabolomic profiling using a combination of high-throughput liquid and gas chromatography-based mass spectrometry on a total of 69 patient-derived glioma specimens, this report documents the discovery of a parallel pathway involving cysteine catabolism that results in the accumulation of cysteine sulfinic acid (CSA) in glioblastoma. These studies identified CSA to rank as one of the top metabolites differentiating glioblastoma from low-grade glioma. There was strong intratumoral concordance of CSA levels with expression of its biosynthetic enzyme cysteine dioxygenase 1 (CDO1). Studies designed to determine the biologic consequence of this metabolic pathway identified its capacity to inhibit oxidative phosphorylation in glioblastoma cells, which was determined by decreased cellular respiration, decreased ATP production, and increased mitochondrial membrane potential following pathway activation. CSA-induced attenuation of oxidative phosphorylation was attributed to inhibition of the regulatory enzyme pyruvate dehydrogenase. Studies performed in vivo abrogating the CDO1/CSA axis using a lentiviral-mediated short hairpin RNA approach resulted in significant tumor growth inhibition in a glioblastoma mouse model, supporting the potential for this metabolic pathway to serve as a therapeutic target. Collectively, we identified a novel, targetable metabolic pathway involving cysteine catabolism contributing to the growth of aggressive high-grade gliomas. These findings serve as a framework for future investigations designed to more comprehensively determine the clinical application of this metabolic pathway and its contributory role in tumorigenesis.

Indexed as

Metabolic Networks and PathwaysAnimalsBrain NeoplasmsCell Line, TumorCysteineCysteine DioxygenaseDisease Models, AnimalEnzyme ActivationGene ExpressionGlioblastomaHumansMiceMice, KnockoutMitochondriaNeoplasm GradingPyruvate Dehydrogenase ComplexCDO1 protein, humanCysteineCysteine Dioxygenasecysteine sulfinic acidPyruvate Dehydrogenase Complex

Identifiers

PMID24351290
PMCPMC5726254
OpenAlexW2116876842

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.