Evidence map›Paper›PMID 25359767›Full record

ArticleOncotarget2014

Human PIF1 helicase supports DNA replication and cell growth under oncogenic-stress.

Mary E Gagou, Anil Ganesh, Geraldine Phear, Darren Robinson, Eva Petermann, Angela Cox, Mark Meuth

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  4. G-quadruplexes as a source of vulnerability in BRCA2Proceedings of the National Academy of Sciences of the United States of America · 2025
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  19. Lysine acetylation regulates the activity of nuclear Pif1.The Journal of biological chemistry · 2020
    Article
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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

7 authors at 2 institutions in 1 country.

Mary E GagouAcademic Unit of Molecular Oncology, Department of Oncology, School of Medicine and Biomedical Sciences, University of Sheffield, Sheffield, UK.
Anil GaneshAcademic Unit of Molecular Oncology, Department of Oncology, School of Medicine and Biomedical Sciences, University of Sheffield, Sheffield, UK.
Geraldine PhearAcademic Unit of Molecular Oncology, Department of Oncology, School of Medicine and Biomedical Sciences, University of Sheffield, Sheffield, UK.
Darren RobinsonLight Microscopy Facility, Department of Biomedical Science, University of Sheffield, Firth Court, Sheffield, UK.
Eva PetermannSchool of Cancer Sciences, University of Birmingham, Edgbaston, Birmingham, UK.
Angela CoxAcademic Unit of Molecular Oncology, Department of Oncology, School of Medicine and Biomedical Sciences, University of Sheffield, Sheffield, UK.
Mark MeuthAcademic Unit of Molecular Oncology, Department of Oncology, School of Medicine and Biomedical Sciences, University of Sheffield, Sheffield, UK.
University of Sheffield · GBUniversity of Birmingham · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Unwinding duplex DNA is a critical processing step during replication, repair and transcription. Pif1 are highly conserved non-processive 5'->3' DNA helicases with well-established roles in maintenance of yeast genome stability. However, the function of the sole member of Pif1 family in humans remains unclear. Human PIF1 is essential for tumour cell viability, particularly during replication stress, but is dispensable in non-cancerous cells and Pif1 deficient mice. Here we report that suppression of PIF1 function slows replication fork rates and increases arrested forks during normal cycling conditions. Importantly, PIF1-dependent replication impediments impair S-phase progression and reduce proliferation rates of RAS oncogene-transformed fibroblasts, where replication fork slowing is exacerbated, but not parental, non-cancerous cells. Disrupted fork movement upon PIF1-depletion does not enhance double-stranded break formation or DNA damage responses but affects resumption of DNA synthesis after prolonged replication inhibitor exposure, accompanied by diminished new origin firing and mainly S-phase entry. Taken together, we characterised a functional role for human PIF1 in DNA replication that becomes important for cell growth under oncogenic stress. Given that oncogenes induce high levels of replication stress during the early stages of tumorigenesis, this function of PIF1 could become critical during cancer development.

Indexed as

Cell Growth ProcessesCell Line, TransformedDNA HelicasesDNA ReplicationFibroblastsGenomic InstabilityHCT116 CellsHumansOncogenesras ProteinsRNA, Small InterferingTransfectionDNA HelicasesPIF1 protein, humanras ProteinsRNA, Small Interfering

Identifiers

PMID25359767
PMCPMC4294361
OpenAlexW1910696387

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.