Evidence map›Paper›PMID 23539451›Full record

ArticleCancer research2013

Endothelial cell protein C receptor opposes mesothelioma growth driven by tissue factor.

Shiva Keshava, Sanghamitra Sahoo, Torry A Tucker, Steven Idell, L Vijaya Mohan Rao, Usha R Pendurthi

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Rivaroxaban does not affect growth of human pancreatic tumors in mice.Journal of thrombosis and haemostasis : JTH · 2019
    Article
  6. Tissue Factor and Cancer: Regulation, Tumor Growth, and Metastasis.Seminars in thrombosis and hemostasis · 2019
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Drug development against the hippo pathway in mesothelioma.Translational lung cancer research · 2017
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Hippo/YAP pathway for targeted therapy.Translational lung cancer research · 2014
    Review
  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

6 authors at 1 institution in 1 country.

Shiva KeshavaDepartment of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, Tyler, Texas 75708, USA.
Sanghamitra Sahoo
Torry A Tucker
Steven Idell
L Vijaya Mohan Rao
Usha R Pendurthi
The University of Texas Health Science Center at Tyler · US

Funding

Factor VIIa Interaction with Endothelial Cell Protein C ReceptorR01HL107483 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI LELLA, VIJAYA MOHAN RAO · 2012 to 2019
$2.9M
Tissue Factor-factor Vlla signalingR01HL065500 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI PENDURTHI, USHA R · 2001 to 2010
$1.8M
The role of coagulation cascade proteases in pleural fibrosisK01HL115466 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI TUCKER, TORRY ALLE · 2012 to 2016
$551k
NHLBI NIH HHS HL107483NHLBI NIH HHS HL65550NHLBI NIH HHS K01 HL115466NHLBI NIH HHS R01 HL065500NHLBI NIH HHS R01 HL107483PHS HHS HLPO1076406
6 · The paper itself

Abstract

The procoagulant protein tissue factor (F3) is a powerful growth promoter in many tumors, but its mechanism of action is not well understood. More generally, it is unknown whether hemostatic factors expressed on tumor cells influence tissue factor-mediated effects on cancer progression. In this study, we investigated the influence of tissue factor, endothelial cell protein C receptor (EPCR, PROCR), and protease activated receptor-1 (PAR1, F2R) on the growth of malignant pleural mesothelioma (MPM), using human MPM cells that lack or express tissue factor, EPCR or PAR1, and an orthotopic nude mouse model of MPM. Intrapleural administration of MPM cells expressing tissue factor and PAR1 but lacking EPCR and PAR2 (F2RL1) generated large tumors in the pleural cavity. Suppression of tissue factor or PAR1 expression in these cells markedly reduced tumor growth. In contrast, tissue factor overexpression in nonaggressive MPM cells that expressed EPCR and PAR1 with minimal levels of tissue factor did not increase their limited tumorigenicity. More importantly, ectopic expression of EPCR in aggressive MPM cells attenuated their growth potential, whereas EPCR silencing in nonaggressive MPM cells engineered to overexpress tissue factor increased their tumorigenicity. Immunohistochemical analyses revealed that EPCR expression in tumor cells reduced tumor cell proliferation and enhanced apoptosis. Overall, our results enlighten the mechanism by which tissue factor promotes tumor growth through PAR1, and they show how EPCR can attenuate the growth of tissue factor-expressing tumor cells.

Indexed as

AnimalsAntigens, CDCell Line, TumorCell ProliferationEndothelial Protein C ReceptorGene ExpressionGene Knockdown TechniquesHumansLipoproteinsMesotheliomaMiceMice, NudeNeoplasm TransplantationPleural NeoplasmsReceptor, PAR-1Receptor, PAR-2Antigens, CDEndothelial Protein C Receptorlipoprotein-associated coagulation inhibitorLipoproteinsPROCR protein, humanReceptor, PAR-1Receptor, PAR-2Receptors, Cell SurfaceRNA, Small InterferingTHBD protein, humanThrombomodulinThromboplastin

Identifiers

PMID23539451
PMCPMC3702650
OpenAlexW2119405901

What OpenQuestion holds

Textmetadata
LicenceTDM
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.