Evidence map›Paper›PMID 26573921›Full record

ReviewCancer metastasis reviews2015

Protease-activated receptors (PARs)--biology and role in cancer invasion and metastasis.

Marek Z Wojtukiewicz, Dominika Hempel, Ewa Sierko, Stephanie C Tucker, Kenneth V Honn

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

  1. Pooled it
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  13. GPCR Biased Signaling in Cancer.Handbook of experimental pharmacology · 2026
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16 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 2 countries.

Marek Z WojtukiewiczDepartment of Oncology, Medical University of Bialystok, 12 Ogrodowa St., 15-025, Bialystok, Poland. mzwojtukiewicz@gmail.com.
Dominika HempelDepartment of Oncology, Medical University of Bialystok, 12 Ogrodowa St., 15-025, Bialystok, Poland.
Ewa SierkoDepartment of Oncology, Medical University of Bialystok, 12 Ogrodowa St., 15-025, Bialystok, Poland.
Stephanie C TuckerBioactive Lipids Research Program, Department of Pathology-School of Medicine, Detroit, MI, USA.
Kenneth V HonnBioactive Lipids Research Program, Department of Pathology-School of Medicine, Detroit, MI, USA.
Medical University of Białystok · PLWayne State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although many studies have demonstrated that components of the hemostatic system may be involved in signaling leading to cancer progression, the potential mechanisms by which they contribute to cancer dissemination are not yet precisely understood. Among known coagulant factors, tissue factor (TF) and thrombin play a pivotal role in cancer invasion. They may be generated in the tumor microenvironment independently of blood coagulation and can induce cell signaling through activation of protease-activated receptors (PARs). PARs are transmembrane G-protein-coupled receptors (GPCRs) that are activated by a unique proteolytic mechanism. They play important roles in vascular physiology, neural tube closure, hemostasis, and inflammation. All of these agents (TF, thrombin, PARs-mainly PAR-1 and PAR-2) are thought to promote cancer invasion and metastasis at least in part by facilitating tumor cell migration, angiogenesis, and interactions with host vascular cells, including platelets, fibroblasts, and endothelial cells lining blood vessels. Here, we discuss the role of PARs and their activators in cancer progression, focusing on TF- and thrombin-mediated actions. Therapeutic options tailored specifically to inhibit PAR-induced signaling in cancer patients are presented as well.

Indexed as

Blood PlateletsEndothelial CellsEnzyme ActivationHumansNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsNeovascularization, PathologicReceptor, PAR-1Receptor, PAR-2ThrombinThromboplastinTumor MicroenvironmentReceptor, PAR-1Receptor, PAR-2ThrombinThromboplastinCancer invasionMetastasisMicroenvironmentPAR-1PAR-2ThrombinTissue factor

Identifiers

PMID26573921
PMCPMC4661218
OpenAlexW2177587731

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.