Evidence map›Paper›PMID 27713160›Full record

ArticleOncotarget2016

Role of BCL9L in transforming growth factor-β (TGF-β)-induced epithelial-to-mesenchymal-transition (EMT) and metastasis of pancreatic cancer.

Giuseppina Sannino, Nicole Armbruster, Mona Bodenhöfer, Ursula Haerle, Diana Behrens, Malte Buchholz, Ulrich Rothbauer, Bence Sipos, Christian Schmees

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

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  17. The Anti-Inflammatory Effects of Vitamin D in Tumorigenesis.International journal of molecular sciences · 2018
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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

9 authors at 3 institutions in 1 country.

Giuseppina SanninoNatural and Medical Sciences Institute (NMI) at the University of Tuebingen, Tumor Biology Group, Reutlingen, Germany.
Nicole ArmbrusterNatural and Medical Sciences Institute (NMI) at the University of Tuebingen, Tumor Biology Group, Reutlingen, Germany.
Mona BodenhöferNatural and Medical Sciences Institute (NMI) at the University of Tuebingen, Tumor Biology Group, Reutlingen, Germany.
Ursula HaerleNatural and Medical Sciences Institute (NMI) at the University of Tuebingen, Tumor Biology Group, Reutlingen, Germany.
Diana BehrensExperimental Pharmacology and Oncology GmbH, Berlin, Germany.
Malte BuchholzDepartment of Medicine, Division of Gastroenterology, Endocrinology and Metabolism, Philipps University Marburg, Marburg, Germany.
Ulrich RothbauerPharmaceutical Biotechnology, University of Tuebingen, Tuebingen, Germany.
Bence SiposInstitute of Pathology, University of Tuebingen, Tuebingen, Germany.
Christian SchmeesNatural and Medical Sciences Institute (NMI) at the University of Tuebingen, Tumor Biology Group, Reutlingen, Germany.
Natural and Medical Sciences Institute · DEUniversity of Tübingen · DEPhilipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) has a low overall survival rate, which is approximately 20% during the first year and decreases to less than 6% within five years of the disease. This is due to premature dissemination accompanied by a lack of disease-specific symptoms during the initial stages. Additionally, to date there are no biomarkers for an early prognosis available.A growing number of studies indicate that epithelial to mesenchymal transition (EMT), triggered by WNT-, TGF-β- and other signaling pathways is crucial for the initiation of the metastatic process in PDAC. Here we show, that BCL9L is up-regulated in PDAC cell lines and patient tissue compared to non-cancer controls. RNAi-induced BCL9L knockdown negatively affected proliferation, migration and invasion of pancreatic cancer cells. On a molecular basis, BCL9L depletion provoked an increment of E-cadherin protein levels, with concomitant increase of β-catenin retention at the plasma membrane. This is linked to the induction of a strong epithelial phenotype in pancreatic cancer cells upon BCL9L knockdown even in the presence of the EMT-inducer TGF-β. Finally, xenograft mouse models of pancreatic cancer revealed a highly significant reduction in the number of liver metastases upon BCL9L knockdown. Taken together, our findings underline the key importance of BCL9L for EMT and thus progression and metastasis of pancreatic cancer cells. Direct targeting of this protein might be a valuable approach to effectively antagonize invasion and metastasis of PDAC.

Indexed as

Adherens JunctionsAnimalsbeta CateninCadherinsCell Line, TumorCell MembraneCell MovementCell ProliferationDisease Models, AnimalEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeterograftsHumansMiceNeoplasm MetastasisBCL9 protein, humanbeta CateninCadherinsNeoplasm ProteinsTranscription FactorsTransforming Growth Factor betaBCL9LE-cadherinEMTpancreatic cancerβ-catenin

Identifiers

PMID27713160
PMCPMC5342010
OpenAlexW2529032812

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.