Evidence map›Paper›PMID 29782654›Full record

ArticleFEBS letters2018

DDX3X RNA helicase affects breast cancer cell cycle progression by regulating expression of KLF4.

Ester Cannizzaro, Andrew John Bannister, Namshik Han, Andrej Alendar, Tony Kouzarides

Open access · hybridAbstract read
In one paragraph

Article in FEBS letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

33 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  4. Role of DEAD/DEAH-box helicases in immunity, infection and cancers.Cell communication and signaling : CCS · 2025
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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

5 authors at 1 institution in 1 country.

Ester CannizzaroDepartment of Pathology and Gurdon Institute, University of Cambridge, Cambridge, UK.
Andrew John BannisterDepartment of Pathology and Gurdon Institute, University of Cambridge, Cambridge, UK.
Namshik HanDepartment of Pathology and Gurdon Institute, University of Cambridge, Cambridge, UK.
Andrej AlendarDepartment of Pathology and Gurdon Institute, University of Cambridge, Cambridge, UK.
Tony KouzaridesDepartment of Pathology and Gurdon Institute, University of Cambridge, Cambridge, UK.
Wellcome/Cancer Research UK Gurdon Institute · GB

Funding

Cancer Research UK 10827Cancer Research UK 17001Cancer Research UK C6946/A14492Cancer Research UK RG17001Wellcome TrustWellcome Trust 092096
6 · The paper itself

Abstract

DDX3X is a multifunctional RNA helicase with documented roles in different cancer types. Here, we demonstrate that DDX3X plays an oncogenic role in breast cancer cells by modulating the cell cycle. Depletion of DDX3X in MCF7 cells slows cell proliferation by inducing a G1 phase arrest. Notably, DDX3X inhibits expression of Kruppel-like factor 4 (KLF4), a transcription factor and cell cycle repressor. Moreover, DDX3X directly interacts with KLF4 mRNA and regulates its splicing. We show that DDX3X-mediated repression of KLF4 promotes expression of S-phase inducing genes in MCF7 breast cancer cells. These findings provide evidence for a novel function of DDX3X in regulating expression and downstream functions of KLF4, a master negative regulator of the cell cycle.

Indexed as

Breast NeoplasmsCell CycleCell ProliferationCells, CulturedDEAD-box RNA HelicasesFemaleGene Expression Regulation, NeoplasticHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMCF-7 CellsDDX3X protein, humanDEAD-box RNA HelicasesKLF4 protein, humanKruppel-Like Factor 4Kruppel-Like Transcription Factorsbreast cancercell cycleDDX3XKLF4RNA helicase

Identifiers

PMID29782654
PMCPMC6100109
OpenAlexW2804443103

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.