Evidence map›Paper›PMID 19891966›Full record

ArticleExperimental cell research2010

Activated protein C enhances cell motility of endothelial cells and MDA-MB-231 breast cancer cells by intracellular signal transduction.

Mark W Gramling, Lea M Beaulieu, Frank C Church

Open access · greenAbstract read
In one paragraph

Article in Experimental cell research, 2010. 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
1.2field-weighted citation impact, top 21% 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, 30 citations in OpenAlex.

  1. Aflatoxin B1 decreased flesh flavor and inhibited muscle development in grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2024
    Article
  2. Article
  3. Review
  4. Article
  5. Activated Protein C in Cutaneous Wound Healing: From Bench to Bedside.International journal of molecular sciences · 2019
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
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  14. Article
  15. Article
  16. [Advances on mechanisms of coagulation with non-small cell lung cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2013
    Review
  17. Monocytes mediate metastatic breast tumor cell adhesion to endothelium under flow.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    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

3 authors at 1 institution in 1 country.

Mark W GramlingDepartments of Pathology and Laboratory Medicine, The University of North Carolina at Chapel Hill, School of Medicine, Chapel Hill, NC 27599-7035, USA.
Lea M Beaulieu
Frank C Church
University of North Carolina at Chapel Hill · US

Funding

INHIBITION OF FACTOR X ACTIVATION BY HEPARIN-ATR01HL032656 · NHLBI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI CHURCH, FRANK C · 1985 to 2004
$1.0M
p16INK4a, Senescence and Aging in Venous ThromboembolismR21AG031068 · NIA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CHURCH, FRANK C · 2007 to 2009
$419k
Role of the Protein C System in Blood Vessel RepairF31NS054590 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BEAULIEU, LEA M · 2006 to 2006
$26k
NHLBI NIH HHS R01 HL032656NHLBI NIH HHS R01 HL32656NHLBI NIH HHS T32 HL697668NIA NIH HHS R21 AG031068NINDS NIH HHS F31 NS054590
6 · The paper itself

Abstract

Activated protein C (APC), an anticoagulant serine protease, has been shown to have non-hemostatic functions related to inflammation, cell survival, and cell migration. In this study we investigate the mechanism by which APC promotes angiogenesis and breast cancer invasion using ex vivo and in vitro methods. When proteolytically active, APC promotes cell motility/invasion and tube formation of endothelial cells. Ex vivo aortic ring assays verify the role of APC in promoting angiogenesis, which was determined to be dependent on EGFR and MMP activation. Given the capacity of APC to promote angiogenesis and the importance of this process in cancer pathology, we investigated whether the mechanisms by which APC promotes angiogenesis can also promote motility and invasion in the MDA-MB-231 breast cancer cell line. Our results indicate that, extracellularly, APC engages EPCR, PAR-1, and EGFR in order to increase the invasiveness of MDA-MB-231 cells. APC activation of matrix metalloprotease (MMP) -2 and/or -9 is necessary but not sufficient to increase invasion, and APC does not utilize the endogenous plasminogen activation system to increase invasion. Intracellularly, APC activates ERK, Akt, and NFkappaB, but not the JNK pathway to promote MDA-MB-231 cell motility. Similar to the hemostatic protease thrombin, APC has the ability to enhance both endothelial cell motility/angiogenesis and breast cancer cell migration.

Indexed as

AnimalsAntigens, CDBreast NeoplasmsCell Line, TumorCell MovementChemotaxisEndothelial CellsEndothelial Protein C ReceptorEnzyme ActivationErbB ReceptorsGene Expression Regulation, NeoplasticHumansIntracellular SpaceIn Vitro TechniquesMatrix MetalloproteinasesMiceAntigens, CDEndothelial Protein C ReceptorErbB ReceptorsMatrix MetalloproteinasesPhosphatidylinositol 3-KinasesPlasminogenPROCR protein, humanProtein CProto-Oncogene Proteins c-aktReceptor, PAR-1Receptors, Cell Surface

Identifiers

PMID19891966
PMCPMC2812600
OpenAlexW1987640476

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.