Evidence map›Paper›PMID 20371605›Full record

ArticleThe Journal of biological chemistry2010

FOXO3a regulates glycolysis via transcriptional control of tumor suppressor TSC1.

Shikha Khatri, Hasmik Yepiskoposyan, Catherine A Gallo, Preeti Tandon, David R Plas

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. FOXO3: at the crossroads of metabolic, inflammatory, and tumorigenic remodeling in the colon.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Ribosomal Protein S6: A Potential Therapeutic Target against Cancer?International journal of molecular sciences · 2021
    Review
  11. Article
  12. Role of TSC1 in physiology and diseases.Molecular and cellular biochemistry · 2021
    Review
  13. Article
  14. Review
  15. Article
  16. Inflammatory Responses Reprogram TScientific reports · 2019
    Article
  17. Article
  18. FoxO transcription factors in cancer metabolism.Seminars in cancer biology · 2018
    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

5 authors at 1 institution in 1 country.

Shikha KhatriDepartment of Cancer and Cell Biology, University of Cincinnati, Cincinnati, Ohio 45267, USA.
Hasmik Yepiskoposyan
Catherine A Gallo
Preeti Tandon
David R Plas
University of Cincinnati · US

Funding

REGULATION OF CELLULAR GROWTH AND DIFFERENTIATIONT32CA059268 · NCI · UNIVERSITY OF CINCINNATI · PI KHAN, SOHAIB A. · 1993 to 2010
$2.3M
Interrupting Akt-S6K1 metabolic control to enhance apoptotic responses in CMLR01CA133164 · NCI · UNIVERSITY OF CINCINNATI · PI PLAS, DAVID R · 2008 to 2012
$1.3M
Regulation of Cellular Survival, Size and MetabolismK01CA098743 · NCI · UNIVERSITY OF PENNSYLVANIA · PI PLAS, DAVID R · 2003 to 2007
$764k
NCI NIH HHS 2T32 CA059268-11NCI NIH HHS K01 CA098743NCI NIH HHS K01 CA98743NCI NIH HHS R01 CA133164NCI NIH HHS T32 CA059268
6 · The paper itself

Abstract

Akt signal transduction induces coordinated increases in glycolysis and apoptosis resistance in a broad spectrum of cancers. Downstream of Akt, the FoxO transcription factors regulate apoptosis via Bim, but the contributions of FoxOs in regulating Akt-induced glycolysis are not well described. We find that FoxO3a knockdown is sufficient to induce apoptosis resistance in conjunction with elevated glycolysis. Glycolysis in FoxO3a-deficient cells was associated with increased S6K1 phosphorylation and was sensitive to rapamycin, an inhibitor of the mTORC1 pathway that has been linked to glycolysis regulation. We show that mTORC1-dependent glycolysis is increased in FoxO3a knockdown cells due to decreased expression of the TSC1 tumor suppressor that opposes mTORC1 activation. FoxO3a binds to and transactivates the TSC1 promoter, indicating a key role for FoxO3a in regulating TSC1 expression. Together, these data demonstrate that FoxO3a regulates glycolysis downstream of Akt through transcriptional control of Tsc1.

Indexed as

AnimalsCell LineForkhead Box Protein O3Forkhead Transcription FactorsGlycolysisHumansImmunosuppressive AgentsMechanistic Target of Rapamycin Complex 1MiceMultiprotein ComplexesPhosphorylationPromoter Regions, GeneticProteinsProto-Oncogene Proteins c-aktRibosomal Protein S6 KinasesSirolimusForkhead Box Protein O3Forkhead Transcription FactorsFOXO3 protein, humanFoxO3 protein, mouseImmunosuppressive AgentsMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProteinsProto-Oncogene Proteins c-aktRibosomal Protein S6 KinasesSirolimusTOR Serine-Threonine KinasesTranscription FactorsTSC1 protein, humanTsc1 protein, mouseTuberous Sclerosis Complex 1 ProteinTumor Suppressor Proteins

Identifiers

PMID20371605
PMCPMC2871464
OpenAlexW1975964180

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.