Evidence map›Paper›PMID 23345610›Full record

ArticleScience translational medicine2013

KLF6-SV1 drives breast cancer metastasis and is associated with poor survival.

Raheleh Hatami, Anieta M Sieuwerts, Sudeh Izadmehr, Zhong Yao, Rui Fang Qiao, Luena Papa, Maxime P Look, Marcel Smid, Jessica Ohlssen, Alice C Levine and 6 more

Open access · greenAbstract read
In one paragraph

Article in Science translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 126 citations in OpenAlex.

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  12. Targeting alternative splicing in cancer immunotherapy.Frontiers in cell and developmental biology · 2023
    Review
  13. Integration of TE Induces Cancer Specific Alternative Splicing Events.International journal of molecular sciences · 2022
    Review
  14. Alternative RNA splicing defects in pediatric cancers: new insights in tumorigenesis and potential therapeutic vulnerabilities.Annals of oncology : official journal of the European Society for Medical Oncology · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 1 institution in 1 country.

Raheleh HatamiDepartment of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, NY 10029, USA.
Anieta M Sieuwerts
Sudeh Izadmehr
Zhong Yao
Rui Fang Qiao
Luena Papa
Maxime P Look
Marcel Smid
Jessica Ohlssen
Alice C Levine
Doris Germain
David Burstein
Alexander Kirschenbaum
Analisa DiFeo
John A Foekens
Goutham Narla
Icahn School of Medicine at Mount Sinai · US

Funding

Mount Sinai Institutes for Clinical and Translational SciencesKL2TR000069 · NCATS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SAMPSON, HUGH A · 2012 to 2014
$2.3M
Small Molecule Activators of PP2A (SMAPs) for Prostate Cancer TherapyR01CA181654 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NARLA, GOUTHAM · 2015 to 2019
$1.9M
Mount Sinai Institutes for Clinical and Translational SciencesKL2RR029885 · NCRR · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MURPHY, BARBARA T. · 2009 to 2011
$1.8M
Howard Hughes Medical InstituteNCATS NIH HHS KL2 TR000069NCATS NIH HHS KL2TR000069NCI NIH HHS R01 CA181654NCRR NIH HHS KL2 RR029885
6 · The paper itself

Abstract

Metastasis is the major cause of cancer mortality. A more thorough understanding of the mechanisms driving this complex multistep process will aid in the identification and characterization of therapeutically targetable genetic drivers of disease progression. We demonstrate that KLF6-SV1, an oncogenic splice variant of the KLF6 tumor suppressor gene, is associated with increased metastatic potential and poor survival in a cohort of 671 lymph node-negative breast cancer patients. KLF6-SV1 overexpression in mammary epithelial cell lines resulted in an epithelial-to-mesenchymal-like transition and drove aggressive multiorgan metastatic disease in multiple in vivo models. Additionally, KLF6-SV1 loss-of-function studies demonstrated reversion to an epithelial and less invasive phenotype. Combined, these findings implicate KLF6-SV1 as a key driver of breast cancer metastasis that distinguishes between indolent and lethal early-stage disease and provides a potential therapeutic target for invasive breast cancer.

Indexed as

AdultAgedAlternative SplicingAnimalsBreast NeoplasmsCell MovementCell ProliferationCell SurvivalDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansKruppel-Like Factor 6Kruppel-Like Transcription FactorsMiceKLF6 protein, humanKruppel-Like Factor 6Kruppel-Like Transcription FactorsNuclear ProteinsProto-Oncogene ProteinsRNA, MessengerTWIST1 protein, humanTwist-Related Protein 1

Identifiers

PMID23345610
PMCPMC4661785
OpenAlexW2143341082

What OpenQuestion holds

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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.