Evidence map›Paper›PMID 24292671›Full record

ArticleOncogene2014

An in vivo RNAi screen identifies SALL1 as a tumor suppressor in human breast cancer with a role in CDH1 regulation.

J Wolf, K Müller-Decker, C Flechtenmacher, F Zhang, M Shahmoradgoli, G B Mills, J D Hoheisel, M Boettcher

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

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  15. Epigenetic modification ofJournal of Cancer · 2018
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  20. Mutual interaction between BCL6 and miRNAs contributing to the pathogenesis of various cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2015
    Review
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

8 authors at 6 institutions in 2 countries.

J WolfDivision of Functional Genome Analysis, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, Germany.
K Müller-DeckerCore Facility Tumor Models, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, Germany.
C FlechtenmacherInstitute of Pathology, Heidelberg University Hospital, Heidelberg, Germany.
F ZhangDepartment of Systems Biology, MD Anderson Cancer Centre, Houston, TX, USA.
M ShahmoradgoliDepartment of Systems Biology, MD Anderson Cancer Centre, Houston, TX, USA.
G B MillsDepartment of Systems Biology, MD Anderson Cancer Centre, Houston, TX, USA.
J D HoheiselDivision of Functional Genome Analysis, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, Germany.
M BoettcherDivision of Functional Genome Analysis, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, Germany.
DKFZ-ZMBH Alliance · DEThe University of Texas MD Anderson Cancer Center · USCenter for Systems Biology · USGerman Cancer Research Center · DEHeidelberg University · DEUniversity Hospital Heidelberg · DE

Funding

Biological annotation of TCGA dataU01CA168394 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MILLS, GORDON B. · 2012 to 2016
$4.7M
Algorithm and genome-wide database of functional siRNAsR44HG003355 · NHGRI · CELLECTA, INC. · PI CHENCHIK, ALEX · 2007 to 2009
$2.5M
Functionally Validated Lentiviral siRNA librariesR44RR024095 · NCRR · CELLECTA, INC. · PI CHENCHIK, ALEX · 2010 to 2011
$1.9M
NCI NIH HHS U01 CA168394NCRR NIH HHS R44 RR024095NHGRI NIH HHS R44 HG003355
6 · The paper itself

Abstract

The gold standard for determining the tumorigenic potential of human cancer cells is a xenotransplantation into immunodeficient mice. Higher tumorigenicity of cells is associated with earlier tumor onset. Here, we used xenotransplantation to assess the tumorigenic potential of human breast cancer cells following RNA interference-mediated inhibition of over 5000 genes. We identify 16 candidate tumor suppressors, one of which is the zinc-finger transcription factor SALL1. Analyzing this particular molecule in more detail, we show that inhibition of SALL1 correlates with reduced levels of CDH1, an important contributor to epithelial-to-mesenchymal transition. Furthermore, SALL1 expression led to an increased migration and more than twice as many cells expressing a cancer stem cell signature. Also, SALL1 expression correlates with the survival of breast cancer patients. These findings cast new light on a gene that has previously been described to be relevant during embryogenesis, but not carcinogenesis.

Indexed as

AnimalsAntigens, CDBreast NeoplasmsCadherinsCarcinogenesisCell Line, TumorDisease-Free SurvivalEpithelial-Mesenchymal TransitionFemaleGene ExpressionGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansKaplan-Meier EstimateMiceMice, Inbred NODAntigens, CDCadherinsCDH1 protein, humanSALL1 protein, humanTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID24292671
PMCPMC6662585
OpenAlexW2147326210

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.