Evidence map›Paper›PMID 26455321›Full record

ArticleOncogene2016

JRK is a positive regulator of β-catenin transcriptional activity commonly overexpressed in colon, breast and ovarian cancer.

L Pangon, I Ng, M Giry-Laterriere, N Currey, A Morgan, F Benthani, P N Tran, S Al-Sohaily, E Segelov, B L Parker and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  10. Evolution ofMobile DNA · 2020
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  11. Review
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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

16 authors at 5 institutions in 1 country.

L PangonThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, Sydney, New South Wales, Australia.
I NgThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, Sydney, New South Wales, Australia.
M Giry-LaterriereThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, Sydney, New South Wales, Australia.
N CurreyThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, Sydney, New South Wales, Australia.
A MorganThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, Sydney, New South Wales, Australia.
F BenthaniThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, Sydney, New South Wales, Australia.
P N TranThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, Sydney, New South Wales, Australia.
S Al-SohailyThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, Sydney, New South Wales, Australia.
E SegelovSt Vincent's Clinical School, UNSW Medicine, UNSW Australia, Sydney, New South Wales, Australia.
B L ParkerBiological Mass Spectrometry Unit, Garvan Institute of Medical Research, Darlinghurst, Sydney, New South Wales, Australia.
M J CowleyThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, Sydney, New South Wales, Australia.
D C WrightCytogenetics, The Children's Hospital at Westmead, Westmead, New South Wales, Australia.
L St HeapsCytogenetics, The Children's Hospital at Westmead, Westmead, New South Wales, Australia.
L CareyCytogenetics, The Children's Hospital at Westmead, Westmead, New South Wales, Australia.
I RoomanThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, Sydney, New South Wales, Australia.
M R J Kohonen-CorishThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, Sydney, New South Wales, Australia.
Garvan Institute of Medical Research · AUChildren's Hospital at Westmead · AUSt Vincent's Clinic · AUThe Kinghorn Cancer Centre · AUUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The loss of β-catenin inhibitory components is a well-established mechanism of carcinogenesis but β-catenin hyperactivity can also be enhanced through its coactivators. Here we first interrogated a highly validated genomic screen and the largest repository of cancer genomics data and identified JRK as a potential new oncogene and therapeutic target of the β-catenin pathway. We proceeded to validate the oncogenic role of JRK in colon cancer cells and primary tumors. Consistent with a β-catenin activator function, depletion of JRK in several cancer cell lines repressed β-catenin transcriptional activity and reduced cell proliferation. Importantly, JRK expression was aberrantly elevated in 21% of colorectal cancers, 15% of breast and ovarian cancers and was associated with increased expression of β-catenin target genes and increased cell proliferation. This study shows that JRK is required for β-catenin hyperactivity regardless of the adenomatous polyposis coli/β-catenin mutation status and targeting JRK presents new opportunities for therapeutic intervention in cancer.

Indexed as

Gene Expression Regulation, NeoplasticTranscription, GeneticActive Transport, Cell NucleusBase Sequencebeta CateninBreast NeoplasmsCell Line, TumorCell NucleusCell ProliferationColonic NeoplasmsComputer SimulationDNA-Binding ProteinsFemaleHumansMutationNuclear Proteinsbeta CateninDNA-Binding ProteinsJRK protein, humanNuclear ProteinsRNA-Binding Proteins

Identifiers

PMID26455321
OpenAlexW2234160496

What OpenQuestion holds

Textmetadata
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.