Evidence map›Paper›PMID 22983094›Full record

ArticleCell cycle (Georgetown, Tex.)2012

Glucose--a sweet way to die: metabolic switching modulates tumor cell death.

Marion MacFarlane, Gemma L Robinson, Kelvin Cain

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. MedComm · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Immunometabolism: Cellular Metabolism Turns Immune Regulator.The Journal of biological chemistry · 2016
    Review
  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

3 authors at 1 institution in 1 country.

Marion MacFarlaneMRC Toxicology Unit, University of Leicester, Leicester, UK. mm21@le.ac.uk
Gemma L Robinson
Kelvin Cain
University of Leicester · GB

Funding

Medical Research Council MC_U132685863
6 · The paper itself

Abstract

TRAIL, a putative anticancer cytokine, induces extrinsic cell death by activating the caspase cascade directly (Type I cells) via the death-inducing signaling complex (DISC) or indirectly (Type II cells) by caspase-8 cleavage of Bid and activation of the mitochondrial cell death pathway. Cancer cells are characterized by their dependence on aerobic glycolysis, which, although inefficient in terms of ATP production, facilitates tumor metabolism. Our studies show that TRAIL-induced cell death is significantly affected by the metabolic status of the cell. Inhibiting glycolysis with 2-deoxyglucose potentiates TRAIL-induced cell death, whereas glucose deprivation can paradoxically inhibit apoptosis. These conflicting responses to glycolysis inhibition are modulated by the balance between the Akt and AMPK pathways and their subsequent downstream regulation of mTORC1. This results in marked changes in protein translation, in which the equilibrium between anti- and pro-apoptotic Bcl-2 family member proteins is decided by their individual degradation rates. This regulates the mitochondrial cell death pathway and alters its sensitivity not only to TRAIL, but to ABT-737, a Bcl-2 inhibitor. Taken together, our studies show that the sensitivity of cancer cells to apoptosis can be modulated by targeting their unique metabolism in order to enhance sensitivity to apoptotic agents.

Indexed as

AMP-Activated Protein KinasesApoptosisBiphenyl CompoundsDeoxyglucoseGlucoseGlycolysisHEK293 CellsHumansMCF-7 CellsMechanistic Target of Rapamycin Complex 1MitochondriaMultiprotein ComplexesNitrophenolsPiperazinesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2ABT-737AMP-Activated Protein KinasesBiphenyl CompoundsDeoxyglucoseGlucoseMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesNitrophenolsPiperazinesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Receptors, TNF-Related Apoptosis-Inducing LigandSulfonamidesTNF-Related Apoptosis-Inducing LigandTOR Serine-Threonine Kinases

Identifiers

PMID22983094
PMCPMC3507486
OpenAlexW2020070665

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.