Evidence map›Paper›PMID 25416949›Full record

ArticleCell2014

lncRNA directs cooperative epigenetic regulation downstream of chemokine signals.

Zhen Xing, Aifu Lin, Chunlai Li, Ke Liang, Shouyu Wang, Yang Liu, Peter K Park, Li Qin, Yongkun Wei, David H Hawke and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 266 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
266citing papers in PubMed, 2 pooled it
13.9field-weighted citation impact, top 1% 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

266 citing papers in PubMed, 2 syntheses or guidelines pooled it, 465 citations in OpenAlex.

  1. Pooled it
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  16. Long non-coding RNANon-coding RNA research · 2024
    Article
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  20. Review

206 more citing papers are in PubMed but not listed here.

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

13 authors at 2 institutions in 2 countries.

Zhen XingDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Aifu LinDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Chunlai LiDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Ke LiangDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Shouyu WangDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Yang LiuDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Peter K ParkDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Li QinDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Yongkun WeiDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
David H HawkeDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Mien-Chie HungDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Cancer Biology Program, The University of Texas Graduate School of Biomedical Sciences, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Graduate Institute of Cancer Biology and Center for Molecular Medicine, China Medical University, Taichung 404, Taiwan.
Chunru LinDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Cancer Biology Program, The University of Texas Graduate School of Biomedical Sciences, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: clin2@mdanderson.org.
Liuqing YangDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Cancer Biology Program, The University of Texas Graduate School of Biomedical Sciences, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Center for RNA Interference and Non-Coding RNAs, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: lyang7@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Orbitrap Elite High-Resolution Mass Spectrometer for Proteomics and MetabolomicsS10OD012304 · OD · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HAWKE, DAVID H · 2013 to 2013
$877k
Nuclear Architecture, NcRNAs and Epigenetics in Transcriptional Regulation by ERR00DK094981 · NIDDK · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LIN, CHUNRU · 2013 to 2015
$747k
Mechanistic Roles of Long mcRNA-regulated Gene Transcription in Prostate CancerR00CA166527 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI YANG, LIUQING · 2013 to 2015
$684k
NCI NIH HHS 5R00CA166527-03NCI NIH HHS P30 CA016672NCI NIH HHS R00 CA166527NIDDK NIH HHS 4R00DK094981-02NIDDK NIH HHS R00 DK094981NIH HHS S10 OD012304PHS HHS K99/R00
6 · The paper itself

Abstract

lncRNAs are known to regulate a number of different developmental and tumorigenic processes. Here, we report a role for lncRNA BCAR4 in breast cancer metastasis that is mediated by chemokine-induced binding of BCAR4 to two transcription factors with extended regulatory consequences. BCAR4 binding of SNIP1 and PNUTS in response to CCL21 releases the SNIP1's inhibition of p300-dependent histone acetylation, which in turn enables the BCAR4-recruited PNUTS to bind H3K18ac and relieve inhibition of RNA Pol II via activation of the PP1 phosphatase. This mechanism activates a noncanonical Hedgehog/GLI2 transcriptional program that promotes cell migration. BCAR4 expression correlates with advanced breast cancers, and therapeutic delivery of locked nucleic acids (LNAs) targeting BCAR4 strongly suppresses breast cancer metastasis in mouse models. The findings reveal a disease-relevant lncRNA mechanism consisting of both direct coordinated protein recruitment and indirect regulation of transcription factors.

Indexed as

Neoplasm MetastasisAnimalsBreast NeoplasmsCell Line, TumorDNA-Binding ProteinsEpigenesis, GeneticHumansIntracellular Signaling Peptides and ProteinsKruppel-Like Transcription FactorsMiceNuclear Proteinsp300-CBP-Associated Factorp300-CBP Transcription FactorsRNA-Binding ProteinsRNA, Long NoncodingSignal TransductionBCAR4 non-coding RNA, humanDNA-Binding ProteinsGli2 protein, mouseIntracellular Signaling Peptides and ProteinsKruppel-Like Transcription FactorsNuclear Proteinsp300-CBP-Associated Factorp300-CBP Transcription FactorsPPP1R10 protein, humanRNA-Binding ProteinsRNA, Long NoncodingSNIP1 protein, humanZinc Finger Protein Gli2

Identifiers

PMID25416949
PMCPMC4266991
OpenAlexW2000564844

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.