Evidence map›Paper›PMID 26284334›Full record

ArticleBritish journal of cancer2015

ADAM10: a new player in breast cancer progression?

Maeve Mullooly, Patricia M McGowan, Susan A Kennedy, Stephen F Madden, John Crown, Norma O' Donovan, Michael J Duffy

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
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  17. Notch signaling pathway: architecture, disease, and therapeutics.Signal transduction and targeted therapy · 2022
    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

7 authors at 3 institutions in 1 country.

Maeve MulloolyUCD School of Medicine and Medical Science, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland.
Patricia M McGowanUCD School of Medicine and Medical Science, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland.
Susan A KennedySystems Biology Ireland, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland.
Stephen F MaddenNational Institute for Cellular Biotechnology (NICB), Dublin City University, Dublin, Ireland.
John CrownNational Institute for Cellular Biotechnology (NICB), Dublin City University, Dublin, Ireland.
Norma O' DonovanNational Institute for Cellular Biotechnology (NICB), Dublin City University, Dublin, Ireland.
Michael J DuffyUCD School of Medicine and Medical Science, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland.
St. Vincent's University Hospital · IEDublin City University · IEUniversity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe ADAM proteases are best known for their role in shedding the extracellular domain of transmembrane proteins. Among the transmembrane proteins shed by ADAM10 are notch, HER2, E-cadherin, CD44, L1 and the EGFR ligands, EGF and betacellulin. As cleavage of several of these proteins has been implicated in cancer formation and progression, we hypothesised that ADAM10 is also involved in these processes.

methodsADAM10 expression was decreased by RNA interference and the effects of this on cell numbers, invasion and migration were determined. We also examined the effect of ADAM10 inhibition on breast cancer cell line invasion and migration.

resultsUsing the triple-negative (TN) breast cancer cell lines, BT20, MDA-MB-231 and the non-TN cell line MDA-MB-453, knockdown of ADAM10 expression significantly decreased in vitro migration (P<0.01; for each cell line). Similarly, treatment with the ADAM10-selective inhibitor GI254023X reduced migration in the three cell lines (for BT20, P<0.001; for MDA-MB-231, P=0.005; for MDA-MB-453, P=0.023). In contrast, neither knockdown of ADAM10 nor treatment with the ADAM10-selective inhibitor GI254023X significantly affected cell numbers. Using extracts of primary breast cancers, higher levels of ADAM10 were found more frequently in high-grade vs low-grade tumours (P<0.001) and in oestrogen receptor (ER)-negative compared with ER-positive tumours (P=0.005). Analysis of pooled publicly available data sets found that high levels of ADAM10 mRNA were associated with adverse outcome in patients with the basal subtype of breast cancer.

conclusionsBased on our combined cell line and breast cancer extract data, we conclude that ADAM10 is likely to be involved in breast cancer progression, especially in the basal subtype.

Indexed as

ADAM10 ProteinADAM ProteinsAmyloid Precursor Protein SecretasesCell CountCell Line, TumorCell MovementDipeptidesDisease-Free SurvivalDisease ProgressionFemaleGene Knockdown TechniquesHumansHydroxamic AcidsMembrane ProteinsMiddle AgedNeoplasm Invasiveness3-(formylhydroxyamino)-2-(3-phenyl-1-propyl)butanoic acid (2,2-dimethyl-1-methylcarbamoyl-1-propyl)amideADAM10 ProteinADAM10 protein, humanADAM ProteinsAmyloid Precursor Protein SecretasesDipeptidesHydroxamic AcidsMembrane ProteinsNeoplasm ProteinsRNA, Messenger

Identifiers

PMID26284334
PMCPMC4578086
OpenAlexW1789716240

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.