Evidence map›Paper›PMID 23744893›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2013

PAK1 regulates breast cancer cell invasion through secretion of matrix metalloproteinases in response to prolactin and three-dimensional collagen IV.

Leah Rider, Peter Oladimeji, Maria Diakonova

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. A Novel PAK1-Notch1 Axis Regulates Crypt Homeostasis in Intestinal Inflammation.Cellular and molecular gastroenterology and hepatology · 2021
    Article
  12. Article
  13. Penta-1,2,3,4,6-Antioxidants (Basel, Switzerland) · 2019
    Article
  14. The role of collagen in cancer: from bench to bedside.Journal of translational medicine · 2019
    Review
  15. Article
  16. Expansion of BCR/ABL1British journal of haematology · 2017
    Article
  17. Review
  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.

Leah RiderDepartment of Biological Sciences, University of Toledo, 2801 West Bancroft Street, Toledo, Ohio 43606-3390, USA.
Peter Oladimeji
Maria Diakonova
University of Toledo · US

Funding

Role of JAK2-PAK1 interaction in prolactin-dependent signalingR01DK088127 · NIDDK · UNIVERSITY OF TOLEDO · PI DIAKONOVA, MARIA · 2010 to 2014
$1.5M
NIDDK NIH HHS R01 DK088127NIDDK NIH HHS R01 DK88127
6 · The paper itself

Abstract

p21-Activated serine-threonine kinase (PAK1) is implicated in breast cancer. We have shown previously that PAK1 is tyrosyl phosphorylated by prolactin (PRL)-activated Janus tyrosine kinase (JAK2). Although a role for both PRL and PAK1 in breast cancer is widely acknowledged, the mechanism remains poorly understood. In the present study, PRL-activated PAK1 stimulates the invasion of TMX2-28 human breast cancer cells through Matrigel. Three-dimensional (3D) collagen IV stimulates the secretion of the matrix proteases, metalloproteinase (MMP)-1 and -3 that is further enhanced by the PRL-dependent tyrosyl phosphorylation of PAK1. 3D collagen IV also stimulates the expression and secretion of MMP-2, but in contrast to MMP-1 and -3, PRL/PAK1 signaling down-regulates MMP-2 expression and secretion. In contrast, MMP-9 expression and secretion are stimulated by 3D collagen I, not collagen IV, and are not affected by PRL but are down-regulated by PAK1. MMP-1 and -3 are required and MMP-2 contributes to PRL-dependent invasion. ERK1/2 signaling appears to be required for the enhanced expression and secretion of MMP-1 and -3 and enhanced PRL-dependent invasion. p38 MAPK and c-Jun N-terminal kinase 1/2 pathways participate in production of MMP-1 and -3 as well as in PRL/PAK1-dependent cell invasion. Together, these data illustrate the complex interaction between the substratum and PRL/PAK1 signaling in human breast cancer cells and suggest a pivotal role for PRL-dependent PAK1 tyrosyl phosphorylation in MMP secretion.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorCollagen Type IVEnzyme ActivationFemaleGene Expression Regulation, NeoplasticHumansMatrix MetalloproteinasesMitogen-Activated Protein KinasesModels, BiologicalMutant ProteinsNeoplasm InvasivenessNF-kappa Bp21-Activated KinasesPhosphorylationCollagen Type IVMatrix MetalloproteinasesMitogen-Activated Protein KinasesMutant ProteinsNF-kappa Bp21-Activated KinasesPhosphotyrosineProlactin

Identifiers

PMID23744893
PMCPMC3706840
OpenAlexW2016977803

What Socratic holds

Textmetadata
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 Socratic graph.