Evidence map›Paper›PMID 28717230›Full record

ArticleScientific reports2017

Activin signaling is an essential component of the TGF-β induced pro-metastatic phenotype in colorectal cancer.

Jonas J Staudacher, Jessica Bauer, Arundhati Jana, Jun Tian, Timothy Carroll, Georgina Mancinelli, Özkan Özden, Nancy Krett, Grace Guzman, David Kerr and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

44 citing papers in PubMed, 64 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 2 institutions in 2 countries.

Jonas J StaudacherDepartment of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Jessica BauerDepartment of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Arundhati JanaDepartment of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Jun TianDepartment of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Timothy CarrollDepartment of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Georgina MancinelliDepartment of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Özkan ÖzdenDepartment of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Nancy KrettDepartment of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Grace GuzmanDepartment of Pathology, University of Illinois at Chicago, Chicago, IL, 60612, USA.ORCID 0000-0001-7256-7223
David KerrNuffield Division of Clinical Laboratory Sciences, University of Oxford, Oxford, UK.
Paul GrippoDepartment of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Barbara JungDepartment of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, Chicago, IL, 60612, USA. bjung@uic.edu.
University of Illinois Chicago · USUniversity of Oxford · GB

Funding

Mechanism of colon cancer metastasis: combined role of activin and TGF-beta signalingR01CA141057 · NCI · UNIVERSITY OF WASHINGTON · PI JUNG, BARBARA H · 2010 to 2021
$3.0M
NCI NIH HHS R01 CA141057
6 · The paper itself

Abstract

Advanced colorectal cancer (CRC) remains a critical health care challenge worldwide. Various TGF-β superfamily members are important in colorectal cancer metastasis, but their signaling effects and predictive value have only been assessed in isolation. Here, we examine cross-regulation and combined functions of the two most prominent TGF-β superfamily members activin and TGF-β in advanced colorectal cancer. In two clinical cohorts we observed by immune-based assay that combined serum and tissue activin and TGF-β ligand levels predicts outcome in CRC patients and is superior to single ligand assessment. While TGF-β growth suppression is independent of activin, TGF-β treatment leads to increased activin secretion in colon cancer cells and TGF-β induced cellular migration is dependent on activin, indicating pathway cross-regulation and functional interaction in vitro. mRNA expression of activin and TGF-β pathway members were queried in silico using the TCGA data set. Coordinated ligand and receptor expression is common in solid tumors for activin and TGF-β pathway members. In conclusion, activin and TGF-β are strongly connected signaling pathways that are important in advanced CRC. Assessing activin and TGF-β signaling as a unit yields important insights applicable to future diagnostic and therapeutic interventions.

Indexed as

ActivinsCell Line, TumorCell MovementCell ProliferationColorectal NeoplasmsFemaleGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansMaleNeoplasm StagingPrognosisSignal TransductionSurvival AnalysisTransforming Growth Factor betaUp-RegulationActivinsTransforming Growth Factor beta

Identifiers

PMID28717230
PMCPMC5514149
OpenAlexW2735265983

What OpenQuestion 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 OpenQuestion graph.