Evidence map›Paper›PMID 30626007›Full record

ReviewCancers2019

Endothelial Protein C Receptor (EPCR), Protease Activated Receptor-1 (PAR-1) and Their Interplay in Cancer Growth and Metastatic Dissemination.

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

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. Review
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  7. Article
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  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Activated Protein C Ameliorates Diabetic CardiomyopathyFrontiers in cardiovascular medicine · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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, 15-089 Bialystok, Poland. mzwojtukiewicz@gmail.com.
Dominika HempelDepartment of Oncology, Medical University of Bialystok, 15-089 Bialystok, Poland. domhem@wp.pl.ORCID 0000-0003-0587-9790
Ewa SierkoDepartment of Oncology, Medical University of Bialystok, 15-089 Bialystok, Poland. ewa.sierko@iq.pl.ORCID 0000-0001-6661-3182
Stephanie C TuckerBioactive Lipids Research Program, Department of Pathology-School of Medicine, Wayne State University, Detroit, MI 48202, USA. stucker@med.wayne.edu.
Kenneth V HonnKarmanos Cancer Institute, Detroit, MI 48201, USA. k.v.honn@wayne.edu.
Medical University of Białystok · PLWayne State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial protein C receptor (EPCR) and protease activated receptor 1 (PAR-1) by themselves play important role in cancer growth and dissemination. Moreover, interactions between the two receptors are essential for tumor progression. EPCR is a cell surface transmembrane glycoprotein localized predominantly on endothelial cells (ECs). It is a vital component of the activated protein C (APC)-mediated anticoagulant and cytoprotective signaling cascade. PAR-1, which belongs to a family of G protein⁻coupled cell surface receptors, is also widely distributed on endothelial and blood cells, where it plays a critical role in hemostasis. Both EPCR and PAR-1, generally considered coagulation-related receptors, are implicated in carcinogenesis and dissemination of diverse tumor types, and their expression correlates with clinical outcome of cancer patients. Existing data explain some mechanisms by which EPCR/PAR-1 affects cancer growth and metastasis; however, the exact molecular basis of cancer invasion associated with the signaling is still obscure. Here, we discuss the role of EPCR and PAR-1 reciprocal interactions in cancer progression as well as potential therapeutic options targeted specifically to interact with EPCR/PAR-1-induced signaling in cancer patients.

Indexed as

APCcancerEPCRmetastasisPAR-1

Identifiers

PMID30626007
PMCPMC6356956
OpenAlexW2908481998

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.