Evidence map›Paper›PMID 25184678›Full record

ArticleGenes & development2014

ZBTB7A acts as a tumor suppressor through the transcriptional repression of glycolysis.

Xue-Song Liu, Jenna E Haines, Elie K Mehanna, Matthew D Genet, Issam Ben-Sahra, John M Asara, Brendan D Manning, Zhi-Min Yuan

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
–field-weighted citation impact
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

66 citing papers in PubMed, 111 citations in OpenAlex.

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  14. PFKP: More than phosphofructokinase.Advances in cancer research · 2023
    Review
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6 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Xue-Song LiuDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA;
Jenna E HainesDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA;
Elie K MehannaDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA;
Matthew D GenetDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA;
Issam Ben-SahraDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA;
John M AsaraDivision of Signal Transduction, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA.
Brendan D ManningDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA;
Zhi-Min YuanDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA; zyuan@hsph.harvard.edu.
Harvard University · USMassachusetts Department of Public Health · USBeth Israel Deaconess Medical Center · US

Funding

Tuberous Sclerosis-Pathway and PathogenesisP01CA120964 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI David J. Kwiatkowski · 2007 to 2026
$35.9M
MOLECULAR BASIS OF P53 INDUCTION TO DNA DAMAGER01CA085679 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI YUAN, ZHI-MIN · 2001 to 2015
$3.4M
Modulation of p53 function by tyrosine kinase networksR01CA167814 · NCI · HARVARD SCHOOL OF PUBLIC HEALTH · PI YUAN, ZHI-MIN · 2012 to 2016
$1.6M
The role of beclin 1/class III PI-3 kinase and p53 in breast tumorigenesisR01CA125144 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI YUAN, ZHI-MIN · 2008 to 2012
$1.5M
NCI NIH HHS P01 CA120964NCI NIH HHS R01 CA085679NCI NIH HHS R01CA085679NCI NIH HHS R01 CA125144NCI NIH HHS R01CA125144NCI NIH HHS R01 CA167814NCI NIH HHS R01CA167814
6 · The paper itself

Abstract

Elevated glycolysis is a common metabolic trait of cancer, but what drives such metabolic reprogramming remains incompletely clear. We report here a novel transcriptional repressor-mediated negative regulation of glycolysis. ZBTB7A, a member of the POK (POZ/BTB and Krüppel) transcription repressor family, directly binds to the promoter and represses the transcription of critical glycolytic genes, including GLUT3, PFKP, and PKM. Analysis of The Cancer Genome Atlas (TCGA) data sets reveals that the ZBTB7A locus is frequently deleted in many human tumors. Significantly, reduced ZBTB7A expression correlates with up-regulation of the glycolytic genes and poor survival in colon cancer patients. Remarkably, while ZBTB7A-deficient tumors progress exceedingly fast, they exhibit an unusually heightened sensitivity to glycolysis inhibition. Our study uncovers a novel tumor suppressor role of ZBTB7A in directly suppressing glycolysis.

Indexed as

Gene Expression Regulation, NeoplasticGenes, Tumor SuppressorAnimalsCell Line, TumorCells, CulturedDNA-Binding ProteinsFemaleGlycolysisHCT116 CellsHumansMCF-7 CellsMiceNeoplasmsPromoter Regions, GeneticProtein BindingTranscription FactorsDNA-Binding ProteinsTranscription FactorsZBTB7A protein, humanGLUT3glycolysisPFKPPKMtumor suppressorZBTB7A

Identifiers

PMID25184678
PMCPMC4197949
OpenAlexW2033250049

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.