Evidence map›Paper›PMID 27351213›Full record

ArticleBritish journal of cancer2016

Overexpression of the oncostatin-M receptor in cervical squamous cell carcinoma is associated with epithelial-mesenchymal transition and poor overall survival.

Justyna A Kucia-Tran, Valtteri Tulkki, Stephen Smith, Cinzia G Scarpini, Katherine Hughes, Angela M Araujo, Ka Yin Matthew Yan, Jan Botthof, Eduardo Pérez-Gómez, Miguel Quintanilla and 3 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 48 citations in OpenAlex.

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  19. Molecular cancer research : MCR · 2020
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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

13 authors at 4 institutions in 2 countries.

Justyna A Kucia-TranDepartment of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.
Valtteri TulkkiDepartment of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.
Stephen SmithDepartment of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.
Cinzia G ScarpiniDepartment of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.
Katherine HughesDepartment of Veterinary Medicine, University of Cambridge, Cambridge CB3 0ES, UK.
Angela M AraujoDepartment of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.
Ka Yin Matthew YanDepartment of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.
Jan BotthofDepartment of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.
Eduardo Pérez-GómezDepartment of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Madrid 28040, Spain.
Miguel QuintanillaDepartment of Cancer Biology, Instituto de Investigaciones Biomédicas Alberto Sols, Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Madrid 28029, Spain.
Kate CuschieriScottish Human Papilloma Virus Reference Laboratory, Specialist Virology Centre, Royal Infirmary of Edinburgh, Edinburgh EH16 4SA, UK.
Maria M CaffarelDepartment of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.
Nicholas ColemanDepartment of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.
University of Cambridge · GBEdinburgh Royal Infirmary · GBInstituto de Investigaciones Biomédicas Sols-Morreale · ESUniversidad Complutense de Madrid · ES

Funding

Cancer Research UK 13080Medical Research Council MC_U105359875
6 · The paper itself

Abstract

backgroundCopy-number gain of the oncostatin-M receptor (OSMR) occurs frequently in cervical squamous cell carcinoma (SCC) and is associated with adverse clinical outcome. We previously showed that OSMR overexpression renders cervical SCC cells more sensitive to the major ligand oncostatin-M (OSM), which increases migration and invasion in vitro. We hypothesised that a major contribution to this phenotype would come from epithelial-mesenchymal transition (EMT).

methodsWe performed a comprehensive integrated study, involving in vitro cell line studies, in vivo animal models and numerous clinical samples from a variety of anatomical sites.

resultsIn independent sets of cervical, head/neck and lung SCC tissues, OSMR expression levels correlated with multiple EMT-associated phenotypic markers and transcription factors. OSM treatment of OSMR overexpressing cervical SCC cells produced consistent EMT changes and increased tumour sphere formation in suspension culture. In a mouse model, OSMR overexpressing SCC cells treated with OSM showed significant increases in lung colonisation. The biological effects of exogenous OSM were mirrored by highly significant adverse overall survival in cervical SCCs with OSMR overexpression (N=251).

conclusionsOSM:OSMR interactions are able to induce EMT, increased cancer stem cell-like properties and enhanced lung colonisation in SCC cells. These changes are likely to contribute to the highly significant adverse outcome associated with OSMR overexpression in cervical SCCs.

Indexed as

Epithelial-Mesenchymal TransitionSurvival AnalysisAnimalsCarcinoma, Squamous CellCell Line, TumorFemaleHeterograftsHumansJanus Kinase 2MiceNeoplasm MetastasisReceptors, Oncostatin MSTAT3 Transcription FactorUterine Cervical NeoplasmsJAK2 protein, humanJanus Kinase 2Receptors, Oncostatin MSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID27351213
PMCPMC4947707
OpenAlexW2468135612

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.