Evidence map›Paper›PMID 25010866›Full record

ArticleBritish journal of cancer2014

The roles of HOXD10 in the development and progression of head and neck squamous cell carcinoma (HNSCC).

F Hakami, L Darda, P Stafford, P Woll, D W Lambert, K D Hunter

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

35 citing papers in PubMed, 54 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

6 authors at 2 institutions in 2 countries.

F Hakami1] Unit of Oral & Maxillofacial Pathology, School of Clinical Dentistry, University of Sheffield, Sheffield S10 2TA, UK [2] Department of Pathology and Laboratory Medicine, King Abdulaziz Medical City-WR, Jeddah, Saudi Arabia.
L DardaUnit of Oral & Maxillofacial Pathology, School of Clinical Dentistry, University of Sheffield, Sheffield S10 2TA, UK.
P StaffordUnit of Oral & Maxillofacial Pathology, School of Clinical Dentistry, University of Sheffield, Sheffield S10 2TA, UK.
P WollAcademic Unit of Clinical Oncology, University of Sheffield, Sheffield S10 2SJ, UK.
D W LambertUnit of Oral & Maxillofacial Pathology, School of Clinical Dentistry, University of Sheffield, Sheffield S10 2TA, UK.
K D Hunter1] Unit of Oral & Maxillofacial Pathology, School of Clinical Dentistry, University of Sheffield, Sheffield S10 2TA, UK [2] Department of Oral Pathology and Biology, University of Pretoria, Pretoria, South Africa.
University of Sheffield · GBUniversity of Pretoria · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHOX gene expression is altered in many cancers; previous microarray revealed changes in HOX gene expression in head and neck squamous cell carcinoma (HNSCC), particularly HOXD10.

methodsHOXD10 expression was assessed by qPCR and immunoblotting in vitro and by immunohistochemistry (IHC) in tissues. Low-expressing cells were stably transfected with HOXD10 and the phenotype assessed with MTS, migration and adhesion assays and compared with the effects of siRNA knockdown in high-HOXD10-expressing cells. Novel HOXD10 targets were identified using expression microarrays, confirmed by reporter assay, and validated in tissues using IHC.

resultsHOXD10 expression was low in NOKs, high in most primary tumour cells, and low in lymph node metastasis cells, a pattern confirmed using IHC in tissues. Overexpression of HOXD10 decreased cell invasion but increased proliferation, adhesion and migration, with knockdown causing reciprocal effects. There was no consistent effect on apoptosis. Microarray analysis identified several putative HOXD10-responsive genes, including angiomotin (AMOT-p80) and miR-146a. These were confirmed as HOXD10 targets by reporter assay. Manipulation of AMOT-p80 expression resulted in phenotypic changes similar to those on manipulation of HOXD10 expression.

conclusionsHOXD10 expression varies by stage of disease and produces differential effects: high expression giving cancer cells a proliferative and migratory advantage, and low expression may support invasion/metastasis, in part, by modulating AMOT-p80 levels.

Indexed as

AngiomotinsCarcinoma, Squamous CellCell Line, TumorDisease ProgressionGene Expression Regulation, NeoplasticHead and Neck NeoplasmsHomeodomain ProteinsHumansIntercellular Signaling Peptides and ProteinsMembrane ProteinsMicrofilament ProteinsMicroRNAsOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticSquamous Cell Carcinoma of Head and NeckTranscription FactorsAMOT protein, humanAngiomotinsHomeodomain ProteinsHOXD10 protein, humanIntercellular Signaling Peptides and ProteinsMembrane ProteinsMicrofilament ProteinsMicroRNAsMIRN146 microRNA, humanTranscription Factors

Identifiers

PMID25010866
PMCPMC4134504
OpenAlexW2027212425

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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.