Evidence map›Paper›PMID 37072858›Full record

ArticleJournal of experimental & clinical cancer research : CR2023

COMMD3 loss drives invasive breast cancer growth by modulating copper homeostasis.

Janelle L Hancock, Murugan Kalimutho, Jasmin Straube, Malcolm Lim, Irma Gresshoff, Jodi M Saunus, Jason S Lee, Sunil R Lakhani, Kaylene J Simpson, Ashley I Bush and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

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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

12 authors at 6 institutions in 1 country.

Janelle L Hancock *QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, QLD, 4006, Australia.
Murugan Kalimutho *QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, QLD, 4006, Australia.
Jasmin StraubeQIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, QLD, 4006, Australia.
Malcolm LimThe University of Queensland Faculty of Medicine, UQ Centre for Clinical Research and Anatomical Pathology, Pathology Queensland, Herston, QLD, 4029, Australia.
Irma GresshoffThe University of Queensland Faculty of Medicine, UQ Centre for Clinical Research and Anatomical Pathology, Pathology Queensland, Herston, QLD, 4029, Australia.
Jodi M SaunusThe University of Queensland Faculty of Medicine, UQ Centre for Clinical Research and Anatomical Pathology, Pathology Queensland, Herston, QLD, 4029, Australia.
Jason S LeeQIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, QLD, 4006, Australia.
Sunil R LakhaniThe University of Queensland Faculty of Medicine, UQ Centre for Clinical Research and Anatomical Pathology, Pathology Queensland, Herston, QLD, 4029, Australia.
Kaylene J SimpsonVictorian Centre for Functional Genomics, Peter MacCallum Cancer Centre, Melbourne, VIC, 3010, Australia.
Ashley I BushFlorey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia.
Robin L AndersonOlivia Newton-John Cancer Research Institute, Heidelberg, VIC, 3084, Australia. Robin.Anderson@onjcri.org.au.
Kum Kum KhannaQIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, QLD, 4006, Australia. kumkum.khanna@qimrberghofer.edu.au.
QIMR Berghofer Medical Research Institute · AUThe University of Queensland · AUFlorey Institute of Neuroscience and Mental Health · AULa Trobe University · AUPeter MacCallum Cancer Centre · AUTranslational Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDespite overall improvement in breast cancer patient outcomes from earlier diagnosis and personalised treatment approaches, some patients continue to experience recurrence and incurable metastases. It is therefore imperative to understand the molecular changes that allow transition from a non-aggressive state to a more aggressive phenotype. This transition is governed by a number of factors.

methodsAs crosstalk with extracellular matrix (ECM) is critical for tumour cell growth and survival, we applied high throughput shRNA screening on a validated '3D on-top cellular assay' to identify novel growth suppressive mechanisms.

resultsA number of novel candidate genes were identified. We focused on COMMD3, a previously poorly characterised gene that suppressed invasive growth of ER + breast cancer cells in the cellular assay. Analysis of published expression data suggested that COMMD3 is normally expressed in the mammary ducts and lobules, that expression is lost in some tumours and that loss is associated with lower survival probability. We performed immunohistochemical analysis of an independent tumour cohort to investigate relationships between COMMD3 protein expression, phenotypic markers and disease-specific survival. This revealed an association between COMMD3 loss and shorter survival in hormone-dependent breast cancers and in particularly luminal-A-like tumours (ER

conclusionOverall, we found that COMMD3 loss promoted aggressive behaviour in breast cancer cells.

Indexed as

CopperNeoplasmsAdaptor Proteins, Signal TransducingAnimalsCell DifferentiationCell ProliferationGene Expression Regulation, NeoplasticMiceSignal TransductionAdaptor Proteins, Signal TransducingCOMMD3 protein, humanCommd3 protein, mouseCopper3D screenBreast cancerCOMMD3Copper signallingTumour suppressor

Identifiers

PMID37072858
PMCPMC10111822
OpenAlexW4366290722

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.