Evidence map›Paper›PMID 23921961›Full record

ArticlePancreas2014

Proteinase-activated receptors differentially modulate in vitro invasion of human pancreatic adenocarcinoma PANC-1 cells in correlation with changes in the expression of CDC42 protein.

Liora Segal, Liora S Katz, Monica Lupu-Meiri, Hagit Shapira, Judith Sandbank, Marvin C Gershengorn, Yoram Oron

Abstract read
In one paragraph

Article in Pancreas, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

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  6. Altered methylation of specific DNA loci in the liver ofFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
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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 2 institutions in 2 countries.

Liora SegalFrom the *Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel; †Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD; ‡Institute of Pathology, Central Lab, Maccabi, Rehovot, Israel; and §Assaf Harofe Hospital Institute of Pathology and the Department of Pathology, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel.
Liora S Katz
Monica Lupu-Meiri
Hagit Shapira
Judith Sandbank
Marvin C Gershengorn
Yoram Oron
Tel Aviv University · ILNational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Study Of Factors That Induce Differentiation Of Pancreatic Precursor CellsZIADK011007 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI GERSHENGORN, MARVIN · 2009 to 2012
$2.7M
Study Of Factors That Induce Differentiation Of Pancreatic Precursor CellsZ01DK011007 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI GERSHENGORN, MARVIN C · 2002 to 2008
$1.1M
Intramural NIH HHS Z01 DK011007
6 · The paper itself

Abstract

objectivesProteinase-activated receptor-1 (PAR-1) and PAR-2 have been associated with increased invasiveness and metastasis in human malignancies. The role of PAR-3 has been less investigated. We examined the role of PARs in a human pancreatic adenocarcinoma PANC-1 cell line phenotype in vitro.

methodsWe knocked down PAR-1, PAR-2, or PAR-3, whereas empty vector-infected cells served as controls. Specific peptide agonists of PARs were used to stimulate the receptors. In vitro assays of colony formation, migration, and invasion were used to characterize the phenotypes, and Western analysis was used to follow cell division control protein 42 homolog (CDC42) expression.

resultsPAR-1 and PAR-2 knockdowns (KDs) were markedly less, whereas PAR-3 KDs were robustly more migratory and invasive than the controls. Stimulation of PAR-1 or PAR-2 by their peptide agonists increased, whereas PAR-3 agonist reduced the invasion of the control cells. Knockdowns of all three PARs exhibited changes in the expression of CDC42, which correlated with the changes in their invasion. Conversely, stimulation of vector-control cells with PAR-1 or PAR-2 agonists enhanced, whereas PAR-3 agonist reduced the expression of CDC42. In the respective KD cells, the effects of the agonists were abrogated.

conclusionThe expression and/or activation of PARs is linked to the invasiveness of PANC-1 cells in vitro, probably via modulation of the expression of CDC42.

Indexed as

AdenocarcinomaAmino Acid SequenceBlotting, Westerncdc42 GTP-Binding ProteinCell Line, TumorCell MovementCells, CulturedHumansPancreatic NeoplasmsPeptidesReceptor, PAR-1Receptor, PAR-2Receptors, ThrombinRNA Interferencecdc42 GTP-Binding ProteinPeptidesprotease-activated receptor 3Receptor, PAR-1Receptor, PAR-2Receptors, Thrombin

Identifiers

PMID23921961
PMCPMC3843996
OpenAlexW2329640003

What OpenQuestion holds

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Registered trials

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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.