Evidence map›Paper›PMID 25634216›Full record

ReviewCancer research2015

Emerging links between E2F control and mitochondrial function.

Elizaveta V Benevolenskaya, Maxim V Frolov

Abstract readReview
In one paragraph

Review in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
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  5. bioRxiv : the preprint server for biology · 2025
    Article
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  9. Article
  10. Review
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  14. Review
  15. Emerging Roles of Long Non-Coding RNAs in Diabetic Foot Ulcers.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021
    Review
  16. Article
  17. Tumor Milieu Controlled by RB Tumor Suppressor.International journal of molecular sciences · 2020
    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

2 authors at 1 institution in 1 country.

Elizaveta V BenevolenskayaDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois. mfrolov@uic.edu evb@uic.edu.
Maxim V FrolovDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois. mfrolov@uic.edu evb@uic.edu.
University of Illinois Chicago · US

Funding

Rb and Hippo tumor suppressor pathways in differentiationR01GM093827 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FROLOV, MAXIM · 2011 to 2018
$2.2M
RBP2 regulation through differential recruitment to genomic lociR01CA138631 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BENEVOLENSKAYA, ELIZAVETA V · 2010 to 2014
$1.6M
NCI NIH HHS CA138631NCI NIH HHS R01 CA138631NIGMS NIH HHS GM93827NIGMS NIH HHS R01 GM093827
6 · The paper itself

Abstract

The family of E2F transcription factors is the key downstream target of the retinoblastoma tumor suppressor protein (pRB), which is frequently inactivated in human cancer. E2F is best known for its role in cell-cycle regulation and triggering apoptosis. However, E2F binds to thousands of genes and, thus, could directly influence a number of biologic processes. Given the plethora of potential E2F targets, the major challenge in the field is to identify specific processes in which E2F plays a functional role and the contexts in which a particular subset of E2F targets dictates a biologic outcome. Recent studies implicated E2F in regulation of expression of mitochondria-associated genes. The loss of such regulation results in severe mitochondrial defects. The consequences become evident during irradiation-induced apoptosis, where E2F-deficient cells are insensitive to cell death despite induction of canonical apoptotic genes. Thus, this novel function of E2F may have a major impact on cell viability, and it is independent of induction of apoptotic genes. Here, we discuss the implications of these findings in cancer biology.

Indexed as

ApoptosisCell Cycle CheckpointsCell SurvivalE2F Transcription FactorsGene Expression Regulation, NeoplasticHumansMitochondriaNeoplasmsRetinoblastoma ProteinTranscription, GeneticTumor Suppressor Protein p53E2F Transcription FactorsRetinoblastoma ProteinTumor Suppressor Protein p53

Identifiers

PMID25634216
PMCPMC4332890
OpenAlexW2140554630

What OpenQuestion holds

Textmetadata
LicenceTDM
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.