Evidence map›Paper›PMID 19543320›Full record

ArticleOncogene2009

Proteinase-activated receptor 2 expression in breast cancer and its role in breast cancer cell migration.

S Su, Y Li, Y Luo, Y Sheng, Y Su, R N Padia, Z K Pan, Z Dong, S Huang

Abstract read
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

45 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Predictive value of protease-activated receptor-2 (PARJournal of cellular and molecular medicine · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. GPCR Modulation in Breast Cancer.International journal of molecular sciences · 2018
    Review
  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

9 authors at 4 institutions in 2 countries.

S SuResearch Center for Traditional Chinese Medicine Complexity System, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Y Li
Y Luo
Y Sheng
Y Su
R N Padia
Z K Pan
Z Dong
S Huang
Shanghai University of Traditional Chinese Medicine · CNAugusta University · USSecond Military Medical University · CNUniversity of Toledo Medical Center · US

Funding

BACTERIA, SIGNALING &LEUKOCYTE TRANSCRIPTION ACTIVATIONR01AI043524 · NIAID · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI PAN, ZHIXING K · 2000 to 2010
$2.6M
The Regulation of UPA and UPAR in Human Carcinoma CellsR01CA093926 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI HUANG, SHUANG · 2002 to 2010
$2.5M
MAPK-activated protein kinase 2 regulation of endothelial cell migrationR01HL083335 · NHLBI · AUGUSTA UNIVERSITY · PI HUANG, SHUANG · 2008 to 2011
$1.5M
NCI NIH HHS CA093926NCI NIH HHS R01 CA093926NHLBI NIH HHS HL083335NHLBI NIH HHS R01 HL083335NIAID NIH HHS R01 AI043524
6 · The paper itself

Abstract

Proteinase-activated receptor 2 (PAR2) is a G protein-coupled receptor that is activated by trypsin-like proteinases. PAR2 is detected in breast tumor specimens; however, it is not clear how PAR2 level in breast cancer cell/tissues compares with normal cell/tissues. Here, we show the elevation of PAR2 protein level in 76 of 105 breast tumor specimens but only 5 of 24 normal breast tissues. PAR2 level is also higher in breast cancer cell lines than that in normal breast cells and non-cancerous breast cell lines. To determine the role of PAR2 in breast carcinogenesis, we examined the effect of PAR2 agonists on cell proliferation and migration. Our studies show that PAR2 agonists (PAR2-activating peptide and trypsin) are neither potent growth enhancers nor chemoattractants to breast cancer cells. Instead, PAR2 agonists induce significant chemokinesis. PAR2-mediated chemokinesis is G(alphai)-dependent, and inhibiting Src kinase activity or silencing c-Src expression blocks PAR2-mediated chemokinesis. These results suggest that c-Src works downstream of G(alphai) to mediate this PAR2 agonist-induced event. To characterize c-Src effector, we reveal that PAR2 agonists activate JNKs in a Src-dependent manner and that JNK activity is essential for PAR2-mediated chemokinesis. Moreover, PAR2 agonist stimulation leads to paxillin Ser(178) phosphorylation and paxillin(S178A) mutant inhibits PAR2-mediated chemokinesis. In conclusion, our studies show that PAR2 agonists facilitate breast cancer cell chemokinesis through the G(alphai)-c-Src-JNK-paxillin signaling pathway.

Indexed as

Cell MovementBreast NeoplasmsCell Line, TumorChemotaxisCSK Tyrosine-Protein KinaseFemaleGTP-Binding Protein alpha Subunits, Gi-GoHumansJNK Mitogen-Activated Protein KinasesPaxillinProtein-Tyrosine KinasesProto-Oncogene ProteinsReceptor, PAR-2Signal Transductionsrc-Family KinasesTrypsinCSK protein, humanCSK Tyrosine-Protein KinaseGTP-Binding Protein alpha Subunits, Gi-GoJNK Mitogen-Activated Protein KinasesPaxillinProtein-Tyrosine KinasesProto-Oncogene ProteinsPXN protein, humanReceptor, PAR-2src-Family KinasesTrypsin

Identifiers

PMID19543320
PMCPMC2733915
OpenAlexW2069049795

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.