Evidence map›Paper›PMID 25816777›Full record

ArticleOncotarget2015

E2F1 enhances glycolysis through suppressing Sirt6 transcription in cancer cells.

Minghui Wu, Edward Seto, Jingsong Zhang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 86 citations in OpenAlex.

  1. Histone deacetylases in cancer metabolic reprogramming.Experimental & molecular medicine · 2026
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  20. Emerging Therapeutic Potential of SIRT6 Modulators.Journal of medicinal chemistry · 2021
    Review
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 2 institutions in 1 country.

Minghui WuDepartment of Genitourinary Oncology and Department of Cancer Imaging and Metabolism, H Lee Moffitt Cancer Center, Tampa, FL, USA.
Edward SetoDepartment of Molecular Oncology, H Lee Moffitt Cancer Center, Tampa, FL, USA.
Jingsong ZhangDepartment of Genitourinary Oncology and Department of Cancer Imaging and Metabolism, H Lee Moffitt Cancer Center, Tampa, FL, USA.
Moffitt Cancer Center · USMolecular Oncology (United States) · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
Integrative Molecular Epidemiology WorkshopR25CA174664 · NCI · AMERICAN ASSOCIATION FOR CANCER RESEARCH · PI Shelley S Tworoger · 2013 to 2026
$2.8M
NCI NIH HHS P30 CA076292NCI NIH HHS P30-CA076292-11S5NCI NIH HHS R25 CA174664
6 · The paper itself

Abstract

The fast proliferation of cancer cells requires reprogramming of its energy metabolism with aerobic glycolysis as a major energy source. Sirt6, a class III histone deacetylase, has been shown to down regulate glycolysis by inhibiting the expression of several key glycolytic genes. Based on the published study on the metabolic phenotype of E2F1 -/- mice and SIRT6 -/- mice, we hypothesize that E2F1 enhances glycolysis and inhibits the expression of Sirt6. Indeed, over-expressing of E2F1, but not its DNA binding deficient mutant, significantly enhanced glucose uptake and lactate production in bladder and prostate cancer cell lines. E2F1 over-expression also suppressed Sirt6 expression and function. Moreover, E2F1 directly bound to Sirt6 promoter and suppressed Sirt6 promoter activity under both normoxic and hypoxic culture conditions. E2F1 siRNA blocked the up-regulation of E2F1 under hypoxia, increased Sirt6 expression and decreased glycolysis compared to those of scrambled siRNA transected cells. Furthermore, HDAC1 deacetylated E2F1 and diminished its transcription suppression of Sirt6 promoter. Treatment with the HDAC inhibitor, trichostatin A (TSA), suppressed Sirt6 promoter activity with increased binding of acetylated E2F1 to Sirt6 promoter. Mutating the E2F1 binding site on the proximal Sirt6 promoter abolished the suppression of Sirt6 transcription by TSA. These data indicate a novel oncogenic role of E2F1, i.e. enhancing glycolysis by suppressing Sirt6 transcription.

Indexed as

GlycolysisBinding SitesCell HypoxiaCell Line, TumorCell ProliferationE2F1 Transcription FactorGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHistone Deacetylase 1Histone Deacetylase InhibitorsHumansLactic AcidMaleMutationPromoter Regions, GeneticProstatic NeoplasmsE2F1 protein, humanE2F1 Transcription FactorHDAC1 protein, humanHistone Deacetylase 1Histone Deacetylase InhibitorsLactic AcidSIRT6 protein, humanSirtuinsE2F1glycolysisHDAC1metabolismSIRT6

Identifiers

PMID25816777
PMCPMC4484454
OpenAlexW2140356459

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.