Evidence map›Paper›PMID 25260534›Full record

ArticleBreast cancer research : BCR2014

Elevated DDX21 regulates c-Jun activity and rRNA processing in human breast cancers.

Yandong Zhang, Kathleen C Baysac, Lian-Fai Yee, Anthony J Saporita, Jason D Weber

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
1.1field-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

59 citing papers in PubMed, 79 citations in OpenAlex.

  1. RNA Helicase DDX21 Controls CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  7. Role of DEAD/DEAH-box helicases in immunity, infection and cancers.Cell communication and signaling : CCS · 2025
    Review
  8. DDX24 spatiotemporally orchestrates VEGF and Wnt signaling during developmental angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  17. International journal of molecular sciences · 2024
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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 2 institutions in 1 country.

Yandong Zhang
Kathleen C Baysac
Lian-Fai Yee
Anthony J Saporita
Jason D Weber
Washington University in St. Louis · USMolecular Oncology (United States) · US

Funding

INTEGRATION OF ONCOGENIC SIGNALS BY THE NUCLEOLAR ARF-NPM NETWORKR01CA120436 · NCI · WASHINGTON UNIVERSITY · PI WEBER, JASON · 2008 to 2012
$1.6M
NCI NIH HHS 1R01CA120436NCI NIH HHS R01 CA120436
6 · The paper itself

Abstract

introductionThe DDX21 RNA helicase has been shown to be a nucleolar and nuclear protein involved in ribosome RNA processing and AP-1 transcription. DDX21 is highly expressed in colon cancer, lymphomas, and some breast cancers, but little is known about how DDX21 might promote tumorigenesis.

methodsImmunohistochemistry was performed on a breast cancer tissue array of 187 patients. In order to study the subcellular localization of DDX21 in both tumor tissue and tumor cell lines, indirect immunofluorescence was applied. The effect of DDX21 knockdown was measured by cellular apoptosis, rRNA processing assays, soft agar growth and mouse xenograft imaging. AP-1 transcriptional activity was analyzed with a luciferase reporter and bioluminescence imaging, as well as qRT-PCR analysis of downstream target, cyclin D1, to determine the mechanism of action for DDX21 in breast tumorigenesis.

resultsHerein, we show that DDX21 is highly expressed in breast cancer tissues and established cell lines. A significant number of mammary tumor tissues and established breast cancer cell lines exhibit nuclear but not nucleolar localization of DDX21. The protein expression level of DDX21 correlates with cell proliferation rate and is markedly induced by EGF signaling. Mechanistically, DDX21 is required for the phosphorylation of c-Jun on Ser73 and DDX21 deficiency markedly reduces the transcriptional activity of AP-1. Additionally, DDX21 promotes rRNA processing in multiple breast cancer cell lines. Tumor cells expressing high levels of endogenous DDX21 undergo apoptosis after acute DDX21 knockdown, resulting in significant reduction of tumorigenicity in vitro and in vivo.

conclusionsOur findings indicate that DDX21 expression in breast cancer cells can promote AP-1 activity and rRNA processing, and thus, promote tumorigenesis by two independent mechanisms. DDX21 could serve as a marker for a subset of breast cancer patients with higher proliferation potential and may be used as a therapeutic target for a subset of breast cancer patients.

Indexed as

AnimalsBreast NeoplasmsCell Cycle CheckpointsCell Line, TumorCell NucleolusCell NucleusCell ProliferationCell SurvivalCell Transformation, NeoplasticDEAD-box RNA HelicasesFemaleHumansMice, Inbred NODMice, NudeMice, SCIDNeoplasm TransplantationDDX21 protein, humanDEAD-box RNA HelicasesProto-Oncogene Proteins c-junRNA, RibosomalTranscription Factor AP-1

Identifiers

PMID25260534
PMCPMC4303128
OpenAlexW2133516504

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.