Evidence map›Paper›PMID 20935507›Full record

ArticleCell cycle (Georgetown, Tex.)2010

Nitrogen anabolism underlies the importance of glutaminolysis in proliferating cells.

Meng Meng, Shuyang Chen, Taotao Lao, Dongming Liang, Nianli Sang

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

55 citing papers in PubMed, 85 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Targeting glutamine metabolism as a potential target for cancer treatment.Journal of experimental & clinical cancer research : CR · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Stanniocalcin 2 (STC2): a universal tumour biomarker and a potential therapeutical target.Journal of experimental & clinical cancer research : CR · 2022
    Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  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

5 authors at 3 institutions in 1 country.

Meng MengDepartment of Biology, College of Arts & Sciences, Drexel University, Philadelphia, PA, USA.
Shuyang Chen
Taotao Lao
Dongming Liang
Nianli Sang
Drexel University · USThomas Jefferson University · USPhiladelphia University · US

Funding

Repressing HIF-1: targets and mechanismsR01CA129494 · NCI · DREXEL UNIVERSITY · PI SANG, NIANLI · 2008 to 2012
$1.6M
Transactivating of Activity of HIF-1 in tumorigenesisK01CA098809 · NCI · THOMAS JEFFERSON UNIVERSITY · PI SANG, NIANLI · 2003 to 2007
$714k
NCI NIH HHS K01 CA098809NCI NIH HHS K01-CA098809NCI NIH HHS R01 CA129494NCI NIH HHS R01-CA129494
6 · The paper itself

Abstract

Glutaminolysis and Warburg effect are the two most noticeable metabolic features of tumor cells whereas their biological significance in cell proliferation remains elusive. A widely accepted current hypothesis is that tumor cells use glutamine as a preferred carbon source for energy and reducing power, which has been used to explain both glutaminolysis and the Warburg effect. Here we provide evidence to show that supplying nitrogen, not the carbon skeleton, underlies the major biological importance of glutaminolysis for proliferating cells. We show alternative nitrogen supplying mechanisms rescue cell proliferation in glutamine-free media. Particularly, we show that ammonia is sufficient to maintain a long-term survival and proliferation of Hep3B in glutamine-free media. We also observed that nitrogen source restriction repressed carbon metabolic pathways including glucose utilization. Based on these new observations and metabolic pathways well established in published literature, we propose an alternative model that cellular demand for glutamate as a key molecule in nitrogen anabolism is the driving force of glutaminolysis in proliferating cells. Our model suggests that the Warburg effect may be a metabolic consequence secondary to the nitrogen anabolism.

Indexed as

Cell ProliferationMetabolismAlanineAmmoniaAspartic AcidCarbonCell Line, TumorEnergy MetabolismGlucoseGlutamineHumansKetoglutaric AcidsMitochondriaNeoplasmsNitrogenNucleic AcidsAlanineAmmoniaAspartic AcidCarbonGlucoseGlutamineKetoglutaric AcidsNitrogenNucleic Acids

Identifiers

PMID20935507
PMCPMC3047752
OpenAlexW2085325650

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.